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	<description>Blood Donation and Donor Search in India .Health tips and articles . Symptoms , Causes and treament for Diseases. Tips for baby care , Pregnancy and pregnant women, Dieting and healthy food info etc ...Site contains all about your health</description>
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		<title>Coronary angiography Risk Factors</title>
		<link>http://www.jeevanraksha.com/heart/coronary-angiography-risk-factors-89</link>
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		<pubDate>Mon, 13 Dec 2010 10:33:40 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[HEART]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/?p=89</guid>
		<description><![CDATA[Heart ailments are the issues that you might want to stay away from. It’s like as if you are walking with a time bomb that might just go off anytime without you noticing it. Your heart is something you really want to protect from any complications and keeping it healthy is the soundest thing to do. There are times however when it can’t be helped that we experience issues with it probably because of the lifestyle we lead or maybe because we are genetically engineered to have such disease. The latter, you can’t do anything. The best thing to do to prevent such ailments from blowing up on your face is to counter it. The moment that you feel something is wrong with your heart, have yourself checked! Prevention they say is better than cure, and with a heart failure looming ahead it’s only reasonable that you take the road away from it. You don’t want to mess with your heart. Coronary angiography or coronary arteriography is one of the means to check if there are heart complications that a patient is experience. It entails a small tube to be inserted in the blood vessel which will be positioned either [...]]]></description>
			<content:encoded><![CDATA[<p>Heart ailments are the issues that you might want to stay away from. It’s like as if you are walking with a time bomb that might just go off anytime without you noticing it. Your heart is something you really want to protect from any complications and keeping it healthy is the soundest thing to do.</p>
<p>There are times however when it can’t be helped that we experience issues with it probably because of the lifestyle we lead or maybe because we are genetically engineered to have such disease. The latter, you can’t do anything. The best thing to do to prevent such ailments from blowing up on your face is to counter it. The moment that you feel something is wrong with your heart, have yourself checked! Prevention they say is better than cure, and with a heart failure looming ahead it’s only reasonable that you take the road away from it. You don’t want to mess with your heart.</p>
<p>Coronary angiography or coronary arteriography is one of the means to check if there are heart complications that a patient is experience. It entails a small tube to be inserted in the blood vessel which will be positioned either in the heart or a blood vessel supplying the heart. There’s also a dye that will be injected to make the veins visible through an x-ray like procedure.</p>
<p>Just like any procedure that has something to do with the heart, coronary angiography also has its risks. The risk factors however are pretty minimal compared to other procedure. However, there might be instances that the complications can turn fatal if the patient has diabetes or kidney issues. Fatality is also there is the patient is 75 years old and a bit high for women.</p>
<p>These complications may include bleeding, pain or infection on the site where the catheter was inserted. If the person doing the procedure is not that used to it, he might poke or scrape a blood vessel which might cause damage to it.</p>
<p>Since there’s a dye that will be injected on the patient, allergic reactions may be noticed. This dye can also cause damage to the kidneys especially if the patient has a failing kidney. Low blood pressure is also one of the complications this procedure might bring.</p>
<p>Despite these complications, the risk factors are pretty minimal and if there are, they’re not too serious or life-threatening. Whatever it is that you do with your body; there is a corresponding reaction to it although for angiography, these are just normal reactions.</p>
<p>Author bio :</p>
<p>Jennica is the author of this article. To learn more about  <a href="http://www.careurheart.com/heart-care-articles/causes-of-high-trigly-cerides.htm">triglycerides levels</a> and <a href="http://www.stressfocus.com/stress_focus_article/symptoms-of-stress.htm">Stress Symptoms</a> just visit the respective sites.</p>
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		<title>Acute Diarrhoeal Diseases</title>
		<link>http://www.jeevanraksha.com/diseases/diarrhoeal/acute-diarrhoeal-diseases-83</link>
		<comments>http://www.jeevanraksha.com/diseases/diarrhoeal/acute-diarrhoeal-diseases-83#comments</comments>
		<pubDate>Fri, 10 Dec 2010 14:26:31 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[DIARRHOEAL]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/?p=83</guid>
		<description><![CDATA[Introduction When a person has loose or watery stools, he has diarrhea. If mucus and blood can be seen in the stools, he has dysentery. Diarrhea can be mild or serious. It can be acute (Lasting for 3 to 7 day) or chronic (Lasting 3 weeks or more) Social Impact : Diarrhoea disease make a heavy demand on health facilities and national health budgets in developing countries. Almost 30 percent of all persons seeking treatment are estimated to be suffering from a Diarrhoeal illness. Highest incidence is seen in children aged 6 months to 2 years which is commonly called the weaning period. Magnitute : Diarrhoeal  diseases are one of the major causes of childhood mortality and morbidity in developing countries. Where an estimated one thousand episodes occur each year in children under five. According to who, Diarrhoeal diseases caused more than 3 million deaths in 1995, 80 percent them being children under five of all the Diarrhoeal deaths, half are due to acute watery diarrhea, 35 percent due to persistent diarrhea and 15 percent due to dysentery. Primary cause of death in acute diarrhea is dehydration due to loss of fluids and electrolytes. Agent Factors : Bacteria : E. [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Introduction</strong></p>
<p><strong> </strong></p>
<p>When a person has loose or watery stools, he has diarrhea. If mucus and blood can be seen in the stools, he has dysentery.</p>
<p>Diarrhea can be mild or serious. It can be acute (Lasting for 3 to 7 day) or chronic (Lasting 3 weeks or more)</p>
<p><strong>Social Impact :</strong></p>
<p>Diarrhoea disease make a heavy demand on health facilities and national health budgets in developing countries. Almost 30 percent of all persons seeking treatment are estimated to be suffering from a Diarrhoeal illness. Highest incidence is seen in children aged 6 months to 2 years which is commonly called the weaning period.</p>
<p><strong>Magnitute : </strong></p>
<p>Diarrhoeal  diseases are one of the major causes of childhood mortality and morbidity in developing countries. Where an estimated one thousand episodes occur each year in children under five. According to who, Diarrhoeal diseases caused more than 3 million deaths in 1995, 80 percent them being children under five of all the Diarrhoeal deaths, half are due to acute watery diarrhea, 35 percent due to persistent diarrhea and 15 percent due to dysentery. Primary cause of death in acute diarrhea is dehydration due to loss of fluids and electrolytes.</p>
<p><strong>Agent Factors :</strong></p>
<p><strong> Bacteria :</strong> E. coli, Vibrio cholerae, Salmonella, Shigella, Campylobactor Jejuni, yersinia enterocolitica, clostridium difficile, clostridium perfringes, S. Acres, Aeronmonas Hydrophile.</p>
<p><strong>Virus :</strong> Rota virus, Adeno virus, Norwalk virus, Corona virus, Astro virus, Entero virus.</p>
<p><strong> Parasites</strong> : Giardia Lamblia, Entamoeba Histolytica, Balantidium coli, Trichuris Trichura, crypto sporidium, Isospora, Stronglyloides stercoralis.</p>
<p>The most common cause of acute diarrhea in children, younger than 2 years of age is rotavirus.</p>
<p>In older children and adults, a possibility of vibrio cholerae infection should always be kept in mind.</p>
<p><strong>Host factors</strong> :</p>
<p><strong>Age :</strong> Most common in children especially those between 6 months and 2 years. Incidence is highest in the age group 6-11 months, when weaning occurs.</p>
<p><strong>Immunity :</strong> Poor immune status predisposes t infection with agents leading to invasive diarrhea.</p>
<p><strong>Malnutrition :</strong> Repeated diarrhoeal episodes are a major cause of malnutrition and faltering weight gain. On the other hand, under nourished children suffer from long-lasting diarrhea and are at 15-20 times greater risk of dying as compared to a wellnourished child with diarrhoeal illness.</p>
<p>Poverty, prematurity, reduced gastric acidity immunodeficiency, lack of personal and domestic hygiene and incorrect feeding practices are all contributory factors.</p>
<p><strong> Environmental factor :</strong></p>
<p><strong>Season :</strong> Diarrhoea tends to occur during summer and rainy seasons.</p>
<p><strong>Macro-Environment :</strong> Inadequate water supply, lack of sanitary facilities, poor personal and domestic hygiene, Improper food preparation and storage, poor weaning practices, early stopping of breast-feeding and practice of bottle-feeding.</p>
<p><strong> </strong></p>
<p><strong>Mode of transmission : </strong></p>
<p>Infecting organisms usually spread by faeco-oral route either by  contaminated food or water. Hands contaminated with faecal also spread infection directly. Files etc. may also spread organisms.</p>
<p><strong>Incubation period :</strong></p>
<p><strong> </strong></p>
<p>Varies, Depending on the causative organism.</p>
<p><strong>Clinical features</strong> :</p>
<ol>
<li>Loose Motion : Initially watery (Diarrhoea) later n with mucus and/or blood (Dy sentry)<strong> </strong></li>
<li>Abdominal pain<strong>.</strong></li>
<li>Vomiting.<strong> </strong></li>
</ol>
<p><strong> </strong></p>
<ol>
<li>Fever : Usually not present but may be of low grade.<strong> </strong></li>
</ol>
<p><strong>Diagnosis :</strong></p>
<ol>
<li>Leucocytosis</li>
<li>Stool examination : it may reveal.</li>
</ol>
<ul>
<li>Trophozites indicating amoebiasis.</li>
<li>Vibro cholerae is usually seen in hanging drop preparation.</li>
<li>Giardia lamblia</li>
</ul>
<ol>
<li>Stool culture for shigellosis.</li>
</ol>
<p><strong>Management</strong></p>
<ol>
<li>Correction of Dehydration.</li>
</ol>
<ul>
<li>If no signs of Dehydration : Give ample of home available fluids (e.g. Rice and dal water, kanji, Buttermilk, Coconut water, Vegetable soups, Fruit juices along with water. Do not discontinue breast feeding but promote it. Teach the parents to watch for signs of dehydration. give the mother one ORS packet with instruction and demonstration about use. Prompt referral if required.</li>
<li>Mild moderate dehydration : Use oral rehydration solution (ORS)</li>
<li>Severe dehydration : Referral/ intravenous fluids</li>
</ul>
<ol>
<li>Correction of electrolyte imbalance.</li>
<li>Chemotherapy</li>
</ol>
<ul>
<li>Ampicillin, co-trimoxazole for bacillary dysentery.</li>
<li>Tetracycline for V. Cholerae.</li>
<li>Metronidazole/ Tinidazole for Giardiasis / Amoebiasis.</li>
</ul>
<ol>
<li>Anti – Motility drugs like lomotil or loperamide be avoided.</li>
</ol>
<p>For practical management of diarrhea, see appendix</p>
<p><strong>Prevention and Control :</strong></p>
<p><strong> </strong></p>
<ol>
<li><strong>1. </strong><strong>Primary prevention :</strong></li>
</ol>
<p>1.   Health promotion :</p>
<ol>
<li>Health Education about personal hygiene, sanitation and waste disposal, Prevention of fly breeding, food and water hygiene.</li>
<li>Legislation :</li>
</ol>
<p>1)      For quality check on hotels and eating establishments.</p>
<p>2)      Licensing and Certification of vendors and food suppliers.</p>
<p>3)      Health check up of food handlers.</p>
<ol>
<li>Specific protection :
<ol>
<li>Immuno-prophylaxis : Immunization is available against salmonella, Shigella, E-coli and certain virus, but not yet used for mass prophylaxis in out country.</li>
</ol>
</li>
</ol>
<p><strong>Secondary Prevention :</strong></p>
<ol>
<li>Early Diagnosis : Using the tests described above.</li>
<li>Prompt and effective treatment : As outlined above and follow-up to avoid carrier states.</li>
</ol>
<p><strong>Tertiary prevention :</strong></p>
<p>Has no role in this disease.</p>
<p><strong>Homeopathy prevention :</strong></p>
<ul>
<li>Collect information about the case and immediately notify the health authorities.</li>
<li>Health education of family, lay persons food handlers, vendors about diarrhoeal disease, sanitation and waste disposal, prevention of fly breeding, food and water hygiene.</li>
<li>Teaching the mother early recognition of severe dehydration and prompt referral.</li>
<li>Promotion and continuation of breast feeding.</li>
<li>Promotion of home fluids and oral rehdration therapy.</li>
</ul>
<p>Disinfection of water sources.</p>
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		<title>Cholera Disease</title>
		<link>http://www.jeevanraksha.com/diseases/diarrhoeal/cholera-disease-81</link>
		<comments>http://www.jeevanraksha.com/diseases/diarrhoeal/cholera-disease-81#comments</comments>
		<pubDate>Fri, 10 Dec 2010 14:19:36 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[DIARRHOEAL]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/?p=81</guid>
		<description><![CDATA[Introduction Cholera is an acute diarrhoeal disease caused by V. Cholera 01 (Classical or E1 Tor).Cases ranges from symptomless to severe infections. Unless there is rapid replacement of and electrolytes, the case fatality may be as high as 30% to 40%. Problem Statement Global experience of the current pandemic have shown that cholera can get introduced into any country, but create problem only in areas where other acute enteric infections endemic, i.e. where sanitation is defective. Currently the seventh pandemic which began in 1961 in Indonesia is still continuing. This pandemic is due to El Tor vibrio. India got involved in the pandemic in 1964. Currently the larger endemic foci of cholera are found in Maharashtra, Tamilnadu, Karnataka, Delhi, Gujarat and Kerala. These states account for about 80% of reported incidence in the country. Epidemiological Features Choler is both epidemic and epidemic disease. Epidemics of Cholera are characteristically abrupt and often create an acute public health problem. The epidemics reach a peak and subsides gradually as the “force of infection” declines. The “force of infection” is composed of 2 components, namely the force of infection through water and the force of infection through contacts. The seasonal variation differs between countries [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Introduction</strong></p>
<p>Cholera is an acute diarrhoeal disease caused by V. Cholera 01 (Classical or E1 Tor).Cases ranges from symptomless to severe infections. Unless there is rapid replacement of and electrolytes, the case fatality may be as high as 30% to 40%.</p>
<p>Problem Statement</p>
<p>Global experience of the current pandemic have shown that cholera can get introduced into any country, but create problem only in areas where other acute enteric infections endemic, i.e. where sanitation is defective. Currently the seventh pandemic which began in 1961 in Indonesia is still continuing. This pandemic is due to El Tor vibrio. India got involved in the pandemic in 1964.<br />
Currently the larger endemic foci of cholera are found in Maharashtra, Tamilnadu, Karnataka, Delhi, Gujarat and Kerala. These states account for about 80% of reported incidence in the country.</p>
<p><strong>Epidemiological Features</strong></p>
<p>Choler is both epidemic and epidemic disease. Epidemics of Cholera are characteristically abrupt and often create an acute public health problem. The epidemics reach a peak and subsides gradually as the “force of infection” declines.<br />
The “force of infection” is composed of 2 components, namely the force of infection through water and the force of infection through contacts.<br />
The seasonal variation differs between countries and even between regions of same country.</p>
<p><strong>Agent Factors:</strong></p>
<p>a)	Agent : The organism that causes cholerae as V. cholera 0 Group 1 or Vibrio cholerae 01.<br />
Within the o Group 1, Classical and El Tor, have been differentiated Classical and El Tor are further divided into 3 serological types namely, Inaba, Ogawa, Hikojima.</p>
<p>b)	Resistance : V. Cholera are killed :-</p>
<p>•	within 30 minutes by heating at 56 deg. C or within few seconds by boiling.<br />
•	by drying in sunshine as cresol.<br />
•	by coal tar such as cresol.<br />
•	By bleaching powder at 6mg / lit.</p>
<p>They remain viable in ice for 4-6 weeks or longer.</p>
<p>c)	Toxin Production</p>
<p>The vibrios multiply in lumen of small intestine and produces an exotoxin.</p>
<p>d)	Reservoir of infection</p>
<p>The human being is the only known reservoir of cholera infection. He may be a case or carrier.</p>
<p>e)	Infective Material</p>
<p>The immediate source of infection are the stools and vomit of cases and carries. Large no. of  vibrios (about 107 to 109 vibrios per ml of fluid) are present in watery stool of cholera patients.</p>
<p>f)	Infective Dose</p>
<p>Cholera is dose related. A very high dose like 1011 organisms is required to produce the clinical disease.</p>
<p>g)	Period of Communicability</p>
<p>A case of cholera is infectious for period of 7-10 days. Convalescent carries are infectious for 2-3 weeks.<br />
The chronic carries state may last from a month upto 10 years or more.<br />
Carriers in Cholera : A cholera carrier may be defined as an apparently healthy person who is excreting V. Cholerae.</p>
<p>a)	Preclinical or incubatory carrier : 1-5 days.<br />
b)	Convalescent carrier : Patient who have recovered from an attack of cholera – usually 2-3 week.</p>
<p>c)	Contact or healthy carrier : This is the result of subclinical infection contracted through Association with source of infection, be it a case or infected environment. Usually less than 10 days.<br />
d)	Chronic carrier : A chronic carrier stage occurs infrequently.</p>
<p><strong>Host factors :</strong></p>
<p>a)	Age &amp; Sex : Cholera affects all ages &amp; both sexes.<br />
b)	Gastric acidity : The vibrio cholerae destroyed in acidic ph 5 or low.<br />
c)	Population mobility : Movement of population (e.g. pilgrimages marriages, fairs &amp; festivals) results in increased risk of exposure.<br />
d)	Economic status : Incidence of cholera tends to be highest in low socio economic group &amp; this is attributable to poor hygiene.<br />
e)	Immunity : Natural infection confers quits effective immunity.</p>
<p><strong>Environmental Factors :</strong></p>
<p>•	Transmission is readily possible in a community with poor environmental sanitation.<br />
•	Environmental factors of imp. Are contaminated water &amp; food.<br />
•	Files may carry vibrio.<br />
•	Social factors like certain human habits favoruring water &amp; soil pollution, low standard of personal hygiene, lack of education &amp; poor quality of life.</p>
<p><strong>Mode of transmission</strong></p>
<p>a)	Faecally contaminated water : uncontrolled water source such as wells, ponds, streams &amp; rivers pose a great threat.<br />
b)	Contaminated food and drinks<br />
c)	Direct contact : Person to person transmission through contaminated fingers while carelessly handing excreta and vomit of patients and contaminated linen and formites.</p>
<p><strong>Incubation Period</strong> : Few hours upto 5 days but commonly 1-2 days</p>
<p><strong>Clinical Features :</strong></p>
<p>a)	Stage of evacuation : onset abrupt with profuse, painless watery diarrhea followed by vomiting. Patients may pass stools 40 times per day. The stools may have rice water appearance.<br />
b)	Stage of collapse : Patient soon passes in stage of collapse because of dehydration. Classical signs are : sunken eyes, hollow cheeks, scaphoid abdomen, subnormal temp. loss of skin elasticity. The output of urine decreases. Death may occur at this stage due to dehydration and acidosis.</p>
<p>c)	Stage of recovery : If death does not occur, the patient begins to show signs of clinical recovery.</p>
<p><strong>Laboratory Diagnosis of Cholera :</strong></p>
<p>a)	Collection of stools : A fresh specimen of stool should be colleted for laboratory examination.<br />
b)	Vomitus : This is practically never used as the chance of isolating vibrios are much less &amp; there is no advantage.<br />
c)	Water : Samples containing 1-3 liters of suspect water should be collected in sterile bottles (for the filter method), or 9 volumes of the sample water added to 1 volume of 10% peptone water &amp; dispatched to the laboratory by quickest method of transport.<br />
d)	Food samples : Samples of food suspected to be contaminated with vibrio cholerae amounting to 1 to 3 gm. Are collected in transport media &amp; sent to laboratory.<br />
e)	Transportation : The stools should be transported in sterilized Mc Cartney bottles 30ml capacity containing alkaline peptone water or VR medium. The specimen should be transported in alkaline peptone water or Cary – Blair medium if it is collected by rectal swab.<br />
f)	Direct examination : If a microscope with dark illumination is available, it may be possible to diagnose about 80% of the cases within a few minutes &amp; more cases after 5-6 hours incubation in alkaline peptone water. In dark field, the vibrios evoke the image of many shooting stars in a dark sky.<br />
g)	Culture method : 0.5 to 1.0 ml of material is inoculated into peptone water tellurite medium for enrichment. After 4-6 hours subcultured on Bite salt agar medium. After overnight incubation plates are screened under obique illumination for vibrio colonies.<br />
h)	Charaterisation :<br />
1)	Gram stain &amp; motility : Gram negative &amp; curved tods with characteristically scintillating motility in hanging drop preparation are very characteristic of V. cholerae.<br />
2)	Serological tests: Slide agglutination test.<br />
Other tests are    &#8211;  direct haemagglutination test with chicken or<br />
sheep red blood cells<br />
-   Polymyxin B sensitivity test using 50<br />
microgm. discs<br />
-   Sensitivity to cholera phage iv<br />
-   V-p reaction<br />
-    Haemolysin tests</p>
<p><strong>Control cholera</strong></p>
<p>The following account is based on the “Guideline for Cholera Control” proposed by who<br />
1)	Verification of the diagnosis : For specific diagnosis of v. cholerae identify v. cholerae 01 in the stools of the patient.<br />
2)	Notification : Cholera is notifiable disease locally, nationally &amp; internationally. Health workers at all levels should be trained to identify &amp; notify cases immediately to local health authority. Under the international health regulations cholera is notifiable to the WHO within 24 hours of its occurrence by the national government. An area is declared free of cholera when twice the incubation period (i.e. 10 days) has elapsed since the heath, recovery or isolation of the last case.<br />
3)	Early case finding : An aggressive search for cases mild, moderate, severe should be made in community for prompt treatment.<br />
4)	Establishment of treatment center : Midly dehydrated patients should be treated at home with oral rehydration solution. Severely dehydrated patients, requiring intravenous fluids should be transferred to the nearest treatment center or hospital.<br />
5)	Rehydration Therapy : Cholera is now most effectively treated disease. Mortality rates have been about down to 1% by effective rehydration therapy. Rehydration may be oral or intravenous.</p>
<p>Oral Rehydration :</p>
<p>The aim of oral fluid therapy is to prevent dehydration &amp; reduce mortality.<br />
Oral fluid therapy is bases on the observation that glucose give orally enhances the intestinal absorption of salt &amp; water &amp; it is capable or correcting electing electrolytes &amp; water deficit.<br />
The composition of oral rehydration fluids recommended by WHO.</p>
<p>Composition of ORS-BICARBONATES</p>
<p>Ingredients 					Quantity<br />
Sodium chloride 				 3.5 gm<br />
Sodium bicarbonate 				 2.5 gm<br />
Potassium bicarbonate 			 1.5 gm<br />
Glucose 					 20.0 gm<br />
Potable water 					 1 lit.</p>
<p>Composition of ORS-CITRATE</p>
<p>Ingredient 					Quantity<br />
Nacl 						 3.5 gm<br />
Trisodium citrate dehydrate 			 2.9 gm<br />
Kcl 						 1.5 gm<br />
Glucose 					 20.0 gm<br />
Potable water 					 1 litre</p>
<p>Packets of ORS are freely available at all primary health centre, subcentre &amp; hospitals. The contents of packets are to be dissolved in 1 litre of water . the solution should be made fresh daily &amp; used within 24 hours.<br />
If the W.H.O. MIXTURE IS NOT available, a simple mixture of table salt (5g) &amp; sugar (20 g) dissolved in 1 litre of water may be safely used.<br />
Intravenous Rehydration : Requires only in initial cases of severely dehydrated patients who are in shock or unable to drink.<br />
The solutions which are recommended by W.H.O. are :<br />
1.	RINGER LACTATE SOLUTION<br />
2.	DIARRHOEA TREATMENT SOLUTION<br />
Maintenance therapy : the general principle is that the oral fluid intake should be equal to the stool loss.</p>
<p>6)	Adjuncts :</p>
<p>Antibiotics should be given along with ORS as soon as vomiting stops. doxycycline, tetracycline, spectrum can be used.</p>
<p>7)	Epidemiological Investigation :</p>
<p>Epidemiological studies should be undertaken to define extent<br />
of out break &amp; find out modes of transmission can be used.</p>
<p>8 ) 	Sanitation Measures</p>
<p>a)	Water control : All steps should be taken to provide properly treated water or safe water for all purposes (drinking, washing, cooking)<br />
b)	Excreta disposal : Provision of simple, cheap &amp; effective excreta disposal.<br />
c)	Food sanitation : Steps should be taken to improve food sanitation particularly sale of food under hygienic conditions.<br />
d)	Disinfection : The most effective disinfectant is a disinfectant with a Rideal – Walker coefficient of 10 or more, such as cresol.</p>
<p>9)	Chemoprophylaxis :</p>
<p>Mass chemoprophylaxis is not advised for the total community because in order to prevent one serious case of cholera, some 10,000 people must be given the drug.<br />
Chemoprophylaxis is advised only for household contacts or of a closed community in which cholera has occurred.<br />
Tetracycline is the drug of choice for chemoprophylaxis</p>
<p>10)	Vaccination :</p>
<p>Cholera vaccine is the only specific prophylactic available against cholera.<br />
The vaccine employed at present is a saline suspension of approximately 6,000 million each of classical Ogawa &amp; Inaba serotypes of V. cholera 01 per ml, so that each ml of the vaccine contains a total of 12,000 million vibrios. The organisms are killed &amp; preserved by 0.5% phenol.</p>
<p>Dosage : Primary immunization consist of 2 equal doses, injected subcutaneously, at an interval of 4 to 6 weeks.</p>
<p>Dosage 				1st dose	 2nd dose<br />
Adult &amp; children over 10 years	0.5 ml		  0.5 ml<br />
Children aged 2 to 10 years	            0.3 ml		  0.3 ml<br />
Children aged 1 to 2 year 		0.2 ml		  0.2 ml</p>
<p>If 2 doses can not be given a month apart, than a single dose equivalent to the double of the first dose should be given. The vaccine not given to children below 1 year. Boosters are every 6 months.<br />
Reactions : Locally tenderness, swelling, redness &amp; sometimes fever.<br />
Contraindication : Person with previous history of sensitivity reaction.<br />
Protective value : About 50% for a period of 3-6 months.</p>
<p><strong>Homeopathy prevention :</strong></p>
<p>1.	Identification of cases and their notification<br />
2.	Health education – should be directed mainly regarding,</p>
<p>i)	Effectiveness &amp; preparation of ORS<br />
ii)	The benefits of early reporting for prompt treatment.<br />
iii)	Food hygiene practices<br />
iv)	Hand washing after defection &amp; before meals.<br />
v)	Benefits of cooked, hot foods &amp; safe water.</p>
<p>3.	An active and passive surveillance for cases<br />
4.	Distribution of ORS packets.<br />
5.	Purification of water supply &amp; proper excreta disposal.<br />
6.	Ensure cholera vaccination, in people during fairs, festivals and large religious functions.<br />
e.g. Kumbha-melas</p>
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		<title>Hepatitis  E</title>
		<link>http://www.jeevanraksha.com/diseases/leukemia/hepatitis-e-78</link>
		<comments>http://www.jeevanraksha.com/diseases/leukemia/hepatitis-e-78#comments</comments>
		<pubDate>Fri, 10 Dec 2010 14:09:19 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[LEUKEMIA]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/?p=78</guid>
		<description><![CDATA[Formerly known as Hepatitis non A non B. It is self-limiting disease transmitted by water or food contamination by faeces of patients. Incubation period : 2-9 weeks Agent : hepatitis E virus is the causative agent. Host : Mainly young adults, 15-40 years Infection during pregnancy is responsible for abortions, intrauterine death &#38; high perinatal morbidity &#38; mortality. Environmental factors : Open air defecation, unsafe drinking water &#38; poor personal hygiene are responsible factors. Homeopathy prevention. 1. Identification of epidemic, identification of source of infection, notification of disease. 2. Ensuring safe water supply, assistance in chlorination of well in a village. 3. Ensure proper sewage disposal. 4. Education of people about food &#38; personal Hygiene. 5. Promote vaccination against Hepatitis B in high risk population groups.]]></description>
			<content:encoded><![CDATA[<p>Formerly known as Hepatitis non A non B.<br />
It is self-limiting disease transmitted by water or food contamination by faeces of patients.<br />
<strong>Incubation period</strong> : 2-9 weeks</p>
<p><strong>Agent</strong> : hepatitis E virus is the causative agent.</p>
<p><strong>Host</strong> : Mainly young adults, 15-40 years<br />
Infection during pregnancy is responsible for abortions, intrauterine death &amp; high perinatal morbidity &amp; mortality.</p>
<p>Environmental factors : Open air defecation, unsafe drinking water &amp; poor personal hygiene are responsible factors.</p>
<p><strong>Homeopathy prevention</strong>.</p>
<p>1.	Identification of epidemic, identification of source of infection, notification of disease.<br />
2.	Ensuring safe water supply, assistance in chlorination of well in a village.<br />
3.	Ensure proper sewage disposal.<br />
4.	Education of people about food &amp; personal Hygiene.<br />
5.	Promote vaccination against Hepatitis B in high risk population groups.</p>
]]></content:encoded>
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		<title>Hepatitis  C</title>
		<link>http://www.jeevanraksha.com/diseases/hepatitis/hepatitis-c-76</link>
		<comments>http://www.jeevanraksha.com/diseases/hepatitis/hepatitis-c-76#comments</comments>
		<pubDate>Fri, 10 Dec 2010 14:08:36 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[Viral Hepatitis]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/?p=76</guid>
		<description><![CDATA[Mainly transmitted through blood &#38; blood products. Incubation period 6-7 weeks. Clinical illness is mild, usually asymatomatic (50%) with a high rate of (more than 50%) chronic hepatitis, which may lead to cirrhosis of liver or liver cancer. Diagnosis : Clinical diagnosis established in person with signs &#38; symptoms of acute hepatitis by ruling out acute HAV and HBV infection. Anti-HAV blood test available but are costly. Homeopathy prevention : Health education to inform general public about risk of transmitting infection with the use of unsterile equipment.]]></description>
			<content:encoded><![CDATA[<p>Mainly transmitted through blood &amp; blood products.<br />
Incubation period 6-7 weeks.<br />
Clinical illness is mild, usually asymatomatic (50%) with a high rate of (more than 50%) chronic hepatitis, which may lead to cirrhosis of liver or liver cancer.</p>
<p><strong>Diagnosis</strong> : Clinical diagnosis established in person with signs &amp; symptoms of acute hepatitis by ruling out acute HAV and HBV infection.</p>
<p>Anti-HAV blood test available but are costly.</p>
<p>Homeopathy prevention :</p>
<p>Health education to inform general public about risk of transmitting infection with the use of unsterile equipment.</p>
]]></content:encoded>
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		<title>Hepatitis  B</title>
		<link>http://www.jeevanraksha.com/diseases/hepatitis/hepatitis-b-74</link>
		<comments>http://www.jeevanraksha.com/diseases/hepatitis/hepatitis-b-74#comments</comments>
		<pubDate>Fri, 10 Dec 2010 14:07:43 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[Viral Hepatitis]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/?p=74</guid>
		<description><![CDATA[Introduction about Hepatitis  B : Formally known as serum hepatitis hepatitis. Usually, it is an acute self limited infection, which may be either subclinical or symptomatic. In approximately 5 to 15% of cases. Infection may cause progressive liver disease including active hepatitis and hepatocellular carcinoma. Incidence &#38; Prevalence : It is endemic throughout the world. In India carrier rate in general population is 5 to 7%. Agent : Hepatitis B virus is DNA virus, replicates in liver cells. It has three different antigens, surface antigen (HbsAg), a core antigen (HbcAg), and an “e” antigen (HbeAg). Man is the only reservoir of infection Contaminated blood is the main source of infection, although virus has been found in saliva, vaginal secretions and semen of infected person. The virus gets destroyed by sodium hypochlorite and by autoclaving for 30 to 60 minutes. High-risk groups are surgeons, recipients of blood transfusions, laboratory personnel, homosexuals, prostitutes, percutaneous drug abusers &#38; infants of HBV carrier mothers. Mode of transmission : Parenteral : infected blood &#38; blood products through transfusions, dialysis, contaminated syringes &#38; needles, pricks of skin, handing of infected blood, surgical &#38; dental procedures, immunization, traditional tattoing, ear &#38; nose piercing, ritual circumcision, acupuncture etc. [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Introduction about Hepatitis  B</strong> : Formally known as serum hepatitis hepatitis. Usually, it is an acute self limited infection, which may be either subclinical or symptomatic. In approximately 5 to 15% of cases. Infection may cause progressive liver disease including active hepatitis and hepatocellular carcinoma.</p>
<p><strong>Incidence &amp; Prevalence</strong> : It is endemic throughout the world. In India carrier rate in general population is 5 to 7%.</p>
<p><strong>Agent</strong> : Hepatitis B virus is DNA virus, replicates in liver cells. It has three different antigens, surface antigen (HbsAg), a core antigen (HbcAg), and an “e” antigen (HbeAg).<br />
Man is the only reservoir of infection<br />
Contaminated blood is the main source of infection, although virus has been found in saliva, vaginal secretions and semen of infected person.<br />
The virus gets destroyed by sodium hypochlorite and by autoclaving for 30 to 60 minutes.</p>
<p>High-risk groups are surgeons, recipients of blood transfusions, laboratory personnel, homosexuals, prostitutes, percutaneous drug abusers &amp; infants of HBV carrier mothers.</p>
<p><strong>Mode of transmission</strong> :</p>
<p>Parenteral :  infected blood &amp; blood products through transfusions, dialysis, contaminated syringes &amp; needles, pricks of skin, handing of infected blood, surgical &amp; dental procedures, immunization, traditional tattoing, ear &amp; nose piercing, ritual circumcision, acupuncture etc.</p>
<p>Perinatal transmission : The sexually promiscuous, particularly male homosexuals, are at very high risk of infection.</p>
<p>Sexual transmission : The sexually promiscuous, particularly male homosexuals, are at very high risk of infection.</p>
<p>Other : Child to child through cuts or skin infection, some blood sucking arthropods are also suspected.</p>
<p><strong>Incubation period</strong> : 45 to 180 days.</p>
<p><strong>Prevention &amp; control</strong> :</p>
<p>Primary : Vaccines available, 2 types, plasma derived &amp; DNA yeast derived.<br />
Immunization schedule</p>
<p>1st dose    1ml   at elected date<br />
2nd dose   1ml   1 month later<br />
3rd dose    1ml   6 months after the first dose</p>
<p>Children under 10 years – half the dose at the same time interval.<br />
Blood to be screened before transfusion.<br />
Encouraging voluntary blood donation<br />
Adequate sterilization of instruments.<br />
Advise to use barrier method of contraception &amp; no to share razors &amp; brushes to carries.</p>
<p><strong>Homeopathy prevention</strong></p>
<p>1.	Health education about blood-safety, spread of disease<br />
2.	Promotion of safe &amp; hygienic practices and discouraging practice of unhygienic tattooing &amp; circumcision.<br />
3.	Encouraging voluntary blood donation<br />
4.	Adequate sterilization of instruments.<br />
5.	Advise to use barrier method of contraception &amp; not to share razors &amp; brushes with carriers.</p>
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		<title>Hepatitis A</title>
		<link>http://www.jeevanraksha.com/diseases/hepatitis/hepatitis-a-69</link>
		<comments>http://www.jeevanraksha.com/diseases/hepatitis/hepatitis-a-69#comments</comments>
		<pubDate>Wed, 08 Dec 2010 13:52:44 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[Viral Hepatitis]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/disease/?p=69</guid>
		<description><![CDATA[Introduction : Formerly known as “Infective” hepatitis or epidemic jaundice, caused by hepatitis A virus. Although mortally is less (0.1%) patients may be incapacitated for many weeks. Incidence &#38; Prevalence : Exact incidence difficult to calculate due to high proportion of asymptomatic case4s however according to W.H.O. it is 10-50 persons per 1,00,000 population per year. Agent : Hepatitis A virus is an enterovirus, which multiplies only in hepatocytes. Faecal shedding of virus is at it’s highest during the later part of incubation period &#38; early acute phase of illness. The virus is inactivated by ultraviolet rays, by boiling for 5 minutes &#38; autoclaving. It withstands heating &#38; routine chlorination. However, it is destroyed in water by super chlorination (1 to 1.5 ppm chlorine levels). Host : more frequent among children, but affects all ages if infected. Both sexes susceptible. Immunity after attack probably lasts for life. Environmental : Associated with heavy rainfall. Poor sanitation &#38; overcrowding favors the spread. Mode of transmission : Major route is faeco oral transmission (direct from person to person or indirectly from contamination of water, food or milk. rarely can be transmitted from parenteral route (blood &#38; products or skin contamination &#38; sexual route). [...]]]></description>
			<content:encoded><![CDATA[<p>Introduction : Formerly known as “Infective” hepatitis or epidemic jaundice, caused by hepatitis A virus. Although mortally is less (0.1%) patients may be incapacitated for many weeks.<br />
<strong>Incidence &amp; Prevalence</strong> : Exact incidence difficult to calculate due to high proportion of asymptomatic case4s however according to W.H.O. it is 10-50 persons per 1,00,000 population per year.</p>
<p><strong>Agent</strong> : Hepatitis A virus is an enterovirus, which multiplies only in hepatocytes. Faecal shedding of virus is at it’s highest during the later part of incubation period &amp; early acute phase of illness. The virus is inactivated by ultraviolet rays, by boiling for 5 minutes &amp; autoclaving. It withstands heating &amp; routine chlorination. However, it is destroyed in water by super chlorination (1 to 1.5 ppm chlorine levels).</p>
<p><strong>Host</strong> : more frequent among children, but affects all ages if infected. Both sexes susceptible. Immunity after attack probably lasts for life.</p>
<p><strong>Environmental</strong> : Associated with heavy rainfall. Poor sanitation &amp; overcrowding favors the spread.</p>
<p><strong>Mode of transmission</strong> : Major route is faeco oral transmission (direct from person to person or indirectly from contamination of water, food or milk. rarely can be transmitted from parenteral route (blood &amp; products or skin contamination &amp; sexual route).</p>
<p><strong>Incubation period</strong> : 15-45 days</p>
<p><strong>Clinical features of Hepatitis A</strong> : Nonspecific symptoms like fever, chills, headache, fatigue, generalized weakness followed by anorexia, nausea, vomiting, dark urine &amp; jaundice. Many cases are subclinical or asymptomatic.</p>
<p><strong>Diagnosis of Hepatitis A</strong> : demonstration of HAV particles or antigens in the faeces. Demonstration of a rise in anti HAV titre. Detection of ig M antibody to HAV.</p>
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		<title>Anticoagulant substances</title>
		<link>http://www.jeevanraksha.com/blood/anticoagulant-substances-66</link>
		<comments>http://www.jeevanraksha.com/blood/anticoagulant-substances-66#comments</comments>
		<pubDate>Wed, 08 Dec 2010 13:48:19 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[BLOOD]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/disease/?p=66</guid>
		<description><![CDATA[What is Anticoagulant An anticoagulant is a substance that reduce blood clotting. This prevents deep vein thrombosis, pulmonary embolism, myocardial infarction and stroke. substances in Anticoagulant Coumadins : these anticoagulants act by causing a fall in level of these factors VII, IX and X and of prothrombin. Factor VII is the most affected. In Vitro, dicoumarol is quantitatively degraded to salicylic acid, and oral administrations of salicylates are known to give rise to hypoprothrombinaemia. Dicoumarol formation in the intestine from sulphonamides orally administrated has been suggested by some. Heparin. Failure of blood coagulation in anaphylactic shock is due to the presence of excess of heparin in the blood. Heparin was first isolated from the liver, hence the name. it found in extracts of other organs. It maintains the natural fluidity of blood in the blood vessel, the normal concentration in blood being 0’009mg. per 100ml. Heparin is normally secreted by mast cells of connective tissue distributed throughout the body. These mast are characteristically found singly or in clumps, in close proximity to the walls of some blood vessels, or interposed in their lining endothelium. These cells contain numerous heparin granules. In conditions of shock, the heparin content of blood is [...]]]></description>
			<content:encoded><![CDATA[<p><strong>What is Anticoagulant</strong></p>
<p><strong></strong>An anticoagulant is a substance that reduce blood clotting. This prevents deep vein thrombosis, pulmonary embolism, myocardial infarction and stroke.<br />
<strong>substances in Anticoagulant</strong><br />
<strong>Coumadins</strong> :  these anticoagulants act by causing a fall in level of these factors VII, IX and X and of prothrombin. Factor VII is the most affected. In Vitro, dicoumarol is quantitatively degraded to salicylic acid, and oral administrations of salicylates are known to give rise to hypoprothrombinaemia. Dicoumarol  formation in the intestine from sulphonamides orally administrated has been suggested by some.<br />
<strong>Heparin</strong>.  Failure of blood coagulation in anaphylactic shock is due to the presence of excess of heparin in the  blood. Heparin was first isolated from the liver, hence the name. it found in extracts of other organs. It maintains the natural fluidity of blood in the blood vessel, the normal concentration in blood being 0’009mg. per 100ml. Heparin  is normally secreted by mast cells of connective tissue distributed throughout the body. These mast are characteristically found singly or in clumps, in close proximity to the walls of  some blood vessels, or interposed in their lining endothelium. These cells contain numerous heparin granules. In conditions of shock,  the heparin  content of blood is increased 20 to 40 times the normal, and at the same time these mast cells show loss of their granules due to exhaustion. Heparin is though to be a dextrorotary polysaccharide made up of hexosamine and hexuronic acid units containing sulphuric acid ester groups. It prevents coagulation acting mainly as an antithrombin and an inhibitor of thromboplastin generation</p>
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		<title>Fibrinogen deficiency</title>
		<link>http://www.jeevanraksha.com/diseases/haemorrhagic/fibrinogen-deficiency-64</link>
		<comments>http://www.jeevanraksha.com/diseases/haemorrhagic/fibrinogen-deficiency-64#comments</comments>
		<pubDate>Wed, 08 Dec 2010 13:38:10 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[HAEMORRHAGIC]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/disease/?p=64</guid>
		<description><![CDATA[The fibrinogen molecule is 30 times as long as it is broad. This asymmetry is responsible for the increased viscosity of the blood, and the increased rouleaux formation of red cells. Increased sedimentation rate of red cells of the blood occurs when there is increased amount of fibrinogen in the plasma. Fibrinogen is formed principally in the liver, and the plasma normally contains 180 to 400mg. fibrinogen per 100ml. .When fibrinogen concentration falls to 60mg. or less per 100ml. haemorrhage occur. Acquired Fibrinogenopenia may occur in severe liver disease, amyloidosis, malignancy, tuberculosis and many other conditions. Congenital Fibrinogenopenia has been reported in which fibrinogen is either completely absent or greatly reduced. In both type, some diminution of platelets also exist, which is responsible positive tourniquet test and increased bleeding time, patients with no fibrinogen have their blood completely incoagulable; most of them die of blood loss in childhood. Diagnosis : coagulation time prolonged, prothrombin time prolonged, bleeding time frequently prolonged. Fibrinogen coagulates at 580 C; so , if plasma is heated to 600 C and remains clear, the inference is that no fibrinogen is present in plasma. By this test, haemophilia an be differentiated from coagulation defect due to Fibrinogenopenia. [...]]]></description>
			<content:encoded><![CDATA[<p>The fibrinogen molecule is 30 times as long as it is broad. This asymmetry is responsible for the increased viscosity of the blood, and the increased rouleaux formation of red cells. Increased sedimentation rate of red cells of the blood occurs when there is increased amount of  fibrinogen in the plasma. Fibrinogen is formed principally in the liver, and the plasma normally contains 180 to 400mg. fibrinogen per 100ml. .When   fibrinogen concentration falls to 60mg. or less per 100ml. haemorrhage occur. Acquired  Fibrinogenopenia  may occur in severe liver disease, amyloidosis, malignancy, tuberculosis and many other conditions. Congenital Fibrinogenopenia  has been reported in which fibrinogen is either  completely absent or greatly reduced. In both type, some diminution of platelets also exist, which is responsible  positive tourniquet test and increased bleeding time, patients with no fibrinogen have their blood completely incoagulable; most of them die of blood loss in childhood. Diagnosis : coagulation time prolonged, prothrombin time prolonged, bleeding time frequently prolonged. Fibrinogen coagulates at 580 C; so , if plasma is heated to 600 C and remains clear, the inference is that no fibrinogen is present in plasma. By this test, haemophilia an be differentiated from coagulation defect due to Fibrinogenopenia.<br />
     Fibrinolysis  causes significant reduction in fibrinogen content of  blood. This is found to occur on the first day of menstruation, in some toxaemias of pregnancy, after I.V. typhoid vaccine or mercurial diuretics, in severe shocks due to extensive haemorrhage or burns. It is believed that all these conditions release tissue enzymes capable of activating the fibrinolysin of plasma. Premature    separation of placenta is specially liable to cause fibrinogen preparations are injected. Again in these conditions, hypoprothrombinaemia may accompany the Fibrinogenopenia as will be evident from prolonged prothrombin time.</p>
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		<title>Prothrombin accelerator defects</title>
		<link>http://www.jeevanraksha.com/diseases/haemorrhagic/prothrombin-accelerator-defects-62</link>
		<comments>http://www.jeevanraksha.com/diseases/haemorrhagic/prothrombin-accelerator-defects-62#comments</comments>
		<pubDate>Wed, 08 Dec 2010 13:37:31 +0000</pubDate>
		<dc:creator>Health tips</dc:creator>
				<category><![CDATA[HAEMORRHAGIC]]></category>

		<guid isPermaLink="false">http://www.jeevanraksha.com/disease/?p=62</guid>
		<description><![CDATA[Plasma factor defects. Deficiency of accelerators of prothrombin activity gives rise to haemophilia in which the coagulation time is prolonged. Haemophilia is inherited as a sex-linked recessive character transmitted from affected males to unaffected female conductors. Haemorrhage occurs either spontaneously or from slight trauma. Subcutaneous or intramuscular haemorrhage and bleeding from the mucous membrane of mouth are common. Haemorrhage into the joints is often (haemarthrosis ) characteristic. An absence of the Factor VIII (anti – haemophilic globulin) in the plasma of these patients is the cause of inhibition of prothrombin activation in the first stage of blood coagulation process.]]></description>
			<content:encoded><![CDATA[<p><strong>Plasma factor defects</strong>.  Deficiency of accelerators of prothrombin activity gives rise to haemophilia in which the coagulation time is prolonged. Haemophilia is inherited as a sex-linked recessive character transmitted from affected males to unaffected female conductors. Haemorrhage occurs either spontaneously or from slight trauma. Subcutaneous or intramuscular haemorrhage and bleeding from the mucous membrane of mouth are common. Haemorrhage into the joints is often (haemarthrosis ) characteristic.  An absence of the Factor VIII (anti – haemophilic globulin) in the plasma of these patients is the cause of inhibition of prothrombin activation in the first stage of blood coagulation process.</p>
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