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	<title>Diseases, Disorders information &#187; Medications</title>
	<atom:link href="http://www.disordersinformation.com/category/medications/feed/" rel="self" type="application/rss+xml" />
	<link>http://www.disordersinformation.com</link>
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		<title>Low back pain. Medications</title>
		<link>http://www.disordersinformation.com/2009/12/04/low-back-pain-medications/</link>
		<comments>http://www.disordersinformation.com/2009/12/04/low-back-pain-medications/#comments</comments>
		<pubDate>Fri, 04 Dec 2009 21:23:22 +0000</pubDate>
		<dc:creator>Disorders</dc:creator>
				<category><![CDATA[Low back pain]]></category>
		<category><![CDATA[Medications]]></category>
		<category><![CDATA[low back pain medications]]></category>

		<guid isPermaLink="false">http://www.disordersinformation.com/?p=264</guid>
		<description><![CDATA[Medications: Good study showing statistical power for nonsteroidals, analgesics and muscle relaxants, the use of those has to be individualized.
Physical Therapy: Absolutely, there was just a publication in the Journal Spine and that is referenced in your hand-out from the Paris Task Force, looking at the superiority of physical therapy to inactivity and shortening symptomatic [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Medications: Good study showing statistical power for nonsteroidals, analgesics and muscle relaxants, the use of those has to be individualized.</strong></p>
<p><strong>Physical Therapy:</strong> Absolutely, there was just a publication in the Journal Spine and that is referenced in your hand-out from the Paris Task Force, looking at the superiority of physical therapy to inactivity and shortening symptomatic intervals, particularly active physical therapy, not modality based therapy, manipulation, hot, cold ice packs, but really active physical therapy.<br />
<strong>Low back pain medications:<br />
Muscle relaxants: Soma is a muscle relaxant used to treat pain caused by muscle spasms.</strong><br />
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<strong>Manipulation:</strong> Believe it or not, there is some very compelling evidence to suggest that may help in the acute phase as with any modality, and by that I mean no more than three to four weeks from the time of onset, chronic manipulation has not been shown to impact long-term health care, delivering a positive sense for low back pain, and injections very controversial despite their wide-spread use, and are used in many individuals. There really are very few studies that demonstrate statistical power as far as the ability of injection to shorten the treatment interval.<br />
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		<title>Autoimmune disease in children</title>
		<link>http://www.disordersinformation.com/2008/12/11/autoimmune-disease-in-children/</link>
		<comments>http://www.disordersinformation.com/2008/12/11/autoimmune-disease-in-children/#comments</comments>
		<pubDate>Thu, 11 Dec 2008 00:10:47 +0000</pubDate>
		<dc:creator>Disorders</dc:creator>
				<category><![CDATA[Medications]]></category>

		<guid isPermaLink="false">http://www.disordersinformation.com/2008/12/11/autoimmune-disease-in-children/</guid>
		<description><![CDATA[Autoimmune disease in children. Well, it’s probably more common than we think. Typically we think of this as a disease affecting adolescent females but we have seen it in boys, we have seen it in little children, even as young as two or sometimes even less. Presentation, again, highly variable. They may turn up with [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Autoimmune disease in children. Well, it’s probably more common than we think. Typically we think of this as a disease affecting adolescent females but we have seen it in boys, we have seen it in little children, even as young as two or sometimes even less.</strong> Presentation, again, highly variable. They may turn up with chronic liver disease and all the characteristic usual associations; cirrhosis, portal hypertension. But where we sometimes see it, and it’s very bothersome when it occurs this way, as a cause of actual fulminant liver failure in sub-acute kind of presentation. Some of these little ones will need liver transplantation very rapidly.<br />
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The diagnostic clue is that if you look at the proteins in the blood, the total serum protein is going to be high and the serum albumin is going to be low and the reason for that is that there is a hypergammaglobulinemia. So if you see a low serum albumin, a high total protein and you are beginning to think about chronic liver disease, it might make you think about autoimmune.<br />
Then there is a whole array of <em><strong>diagnostic markers</strong></em> that I am not going to delineate for you; anti-smooth muscle, anti-mitochondrial antibodies, anti-liver-kidney microsomal. You can think about just about any antibody you want to and look for it as part of the way that you prove your diagnosis. Along, of course, with liver biopsy.<br />
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<strong>The treatment, particularly if you are savvy and you make this diagnosis early, is immunosuppression.</strong> The mainstay is still steroids. You might add 6-MP, azathioprine or even some of the newer immunosuppressants to try and control the process. You have to remember that autoimmune diseases, no matter which one it is, are multi-system diseases so whether the presentation is in the liver or somewhere else, you should look at the joints, you look for funny rashes, you look for ulcerative colitis and <a HREF="http://www.disordersinformation.com/2007/11/04/crohns-disease/">Crohn’s disease</a>, diabetes, thyroid problems. So don’t just stop at the liver. Make sure you have really carefully gone through all the other systems that could be involved.<br />
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		<title>Heat stroke</title>
		<link>http://www.disordersinformation.com/2008/12/02/heat-stroke/</link>
		<comments>http://www.disordersinformation.com/2008/12/02/heat-stroke/#comments</comments>
		<pubDate>Tue, 02 Dec 2008 21:25:51 +0000</pubDate>
		<dc:creator>Disorders</dc:creator>
				<category><![CDATA[Medications]]></category>

		<guid isPermaLink="false">http://www.disordersinformation.com/2008/12/02/heat-stroke/</guid>
		<description><![CDATA[Heat stroke is a medical emergency. These patients need very aggressive cooling. This may involve packing them in ice externally. It may involve administering cool fluids to every orifice and IV site to bring down their body temperature rapidly. They need to be fluid resuscitated, they are essentially all dehydrated and vasodilated, and they need [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Heat stroke is a medical emergency. These patients need very aggressive cooling. This may involve packing them in ice externally. It may involve administering cool fluids to every orifice and IV site to bring down their body temperature rapidly. They need to be fluid resuscitated, they are essentially all dehydrated and vasodilated, and they need ongoing supportive care.</strong><br />
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Now there is a specific syndrome in young children that has been reported, of hemorrhagic shock and encephalopathy syndrome. Which is basically unexplained severe hyperthermia in young children without an infectious etiology defined, which is associated with a very significant encephalopathy. These patients develop shock, DIC and actually have a high mortality rate. In the initial series, 100% mortality rate was reported. Now survivors have been reported, but it still does have a high mortality rate. It is uncommon but has been the source of questions in the past.<br />
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Smoke inhalation; another environmental disaster. If you happen to be in a fire you get asphyxiated. Fire consumes oxygen, it leaves what you are breathing to be relatively oxygen-free, and although you are having air exchange you are not getting oxygen to your tissues. You may have a thermal injury, although this is a much less common cause of death, where you actually have flame injury to the tissues. A thermal injury with super-heated environments, gases especially if there is steam involved, you may get airway injury from the high temperatures. This is typically supraglottic. By the time it gets down to your lungs the gases have usually cooled enough that you don’t have burning all the way down your lungs. You may begin to develop airway edema. If you have a child who has stridor following a burn injury, they have soot in their oropharynx, you want to establish an airway quickly before it swells shut. So burns to the lip or nose, soot in the mouth, singed nasal hair, stridor, hoarseness or respiratory distress, are all indications for intubation. Don’t wait and hope that they are going to get better. They are going to get worse before they get better and they need an airway.<br />
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<strong>Carbon monoxide;</strong> combustion releases carbon monoxide. When it’s in a fire it will be associated with soot and other things. You can get carbon monoxide poisoning in other environments. Exhaust systems of furnaces may dysfunction and everyone in the home may in fact have carbon monoxide poisoning. It’s a colorless, odorless gas so they won’t know it until they are losing consciousness or having changes. We are going to talk a little about the pathophysiology, the diagnosis and the therapy. Again, it’s colorless, odorless, non-irritating gas. Sounds like a pretty good way to kill somebody, to me.</p>
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		<title>Obstructive uropathy</title>
		<link>http://www.disordersinformation.com/2008/11/19/obstructive-uropathy/</link>
		<comments>http://www.disordersinformation.com/2008/11/19/obstructive-uropathy/#comments</comments>
		<pubDate>Wed, 19 Nov 2008 14:13:17 +0000</pubDate>
		<dc:creator>Disorders</dc:creator>
				<category><![CDATA[Medications]]></category>

		<guid isPermaLink="false">http://www.disordersinformation.com/2008/11/19/obstructive-uropathy/</guid>
		<description><![CDATA[OBSTRUCTIVE UROPATHY
Obstructive uropathy lends itself to early detection with ultrasonography. Posterior urethral valves or bladder outlet obstructions are the most common of these disorders, but the obstruction may be at any level of the urinary tract.
In all cases of obstructive uropathy, the rationale behind treatment is that the obstruction itself will lead to permanent renal [...]]]></description>
			<content:encoded><![CDATA[<p><strong>OBSTRUCTIVE UROPATHY</strong></p>
<p>Obstructive uropathy lends itself to early detection with ultrasonography. Posterior urethral valves or bladder outlet obstructions are the most common of these disorders, but the obstruction may be at any level of the urinary tract.<br />
In all cases of obstructive uropathy, the rationale behind treatment is that the obstruction itself will lead to permanent renal damage in the developing fetus. Obstruction of the urinary tract will lead to oligohydramnios and pulmonary hypoplasia, which is usually the cause of death in these neonates. Thus, the rationale for invasive therapy is that it will prevent a potentially fatal sequence of events and, if successful, will lead to a favorable long-term prognosis. Ideal candidates for the procedure are fetuses with isolated anomalies who are found in the second or very early third trimester with progressive oligohydramnios but good remaining renal function.</p>
<p><strong>DIAPHRAGMATIC HERNIA</strong></p>
<p>Diaphragmatic hernia is a serious fetal anomaly with a high perinatal mortality rate. Although it may be associated with other fetal anomalies, more frequently it is isolated. Death of neonates from pulmonary hypoplasia is believed to be due to compression of the normal lung in utero by herniated abdominal contents. Various methods of in utero repair have been proposed, including open fetal surgery. In this procedure, a hysterotomy is performed and the exteriorized fetus undergoes surgery to repair the defect and allow normal lung development.<br />
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		<title>New dermatologic sings and symptoms</title>
		<link>http://www.disordersinformation.com/2008/10/22/new-dermatologic-sings-and-symptoms/</link>
		<comments>http://www.disordersinformation.com/2008/10/22/new-dermatologic-sings-and-symptoms/#comments</comments>
		<pubDate>Wed, 22 Oct 2008 18:01:47 +0000</pubDate>
		<dc:creator>Disorders</dc:creator>
				<category><![CDATA[Medications]]></category>

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Traditional clinical findings in skin presentations of candida infection include erythematous papules and nodules, ecthyma-gangrenosum-like ulcerations and verrucous plaques. Purpura fulminans and disseminated intravascular coagulation were described by Silverman et al in a patient with candida sepsis. Purpura fulminans typically is associated with precipitous development of shock, fever, and [...]]]></description>
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Traditional clinical findings in skin presentations of candida infection include erythematous papules and nodules, ecthyma-gangrenosum-like ulcerations and verrucous plaques. Purpura fulminans and disseminated intravascular coagulation were described by Silverman et al in a patient with candida sepsis. Purpura fulminans typically is associated with precipitous development of shock, fever, and symmetrically distributed purpuric plaques that form when the skin lesions, which initially are petechiae, rapidly coalesce. In the series of patients described by Silverman et al, the biopsy of skin lesions revealed characteristic histologic changes and pseudohyphae and budding yeast cells amid the necrosis deep in the reticular dermis. When the biopsy material was cultured, it yielded Candida tropicalis, the same organism that was also identified from the blood. Silverman et al concluded that purpura fulminans can provide an early diagnostic clue in patients with candida sepsis.<br />
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Hemorrhagic bullae have been described in patients with Candida tropicalis sepsis. In these patients, it is postulated that the release of lytic enzymes by the invading organisms caused destruction of dermal collagen with resultant bullae formation. Candida tropicalis organisms were present in numerous foci within the cavity of the bullae and around surrounding collagen fibers. In immunocompromised patients, Suster and Rosen concluded that the development of bullous skin lesions could be a sign of disseminated candidiasis. Early diagnosis is enhanced by biopsy and histological examination of lesions.<br />
<strong>DIAGNOSIS OF CANDIDEMIA</strong><br />
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The growing importance of fungal species as agents of septicemia-candidemia has resulted in increased efforts to diagnose these infections accurately. Stone et al evaluated the pathogenesis and principles of treatment of Candida species and demonstrated the remarkable efficiency with which the liver cleared candida from venous blood (ratio of 10,000:1); the lungs, striated muscle, and kidneys were less effective but also filtered yeasts from the blood. This phenomenon explains why some suggest that antemortem blood cultures drawn to confirm clinical diagnosis of candidemia should be obtained from a peripheral artery or the right atrium to minimize any influence of tissue filtration. Pizzo and Walsh noted that approximately 40% to 60% of patients with proven hematogenously disseminated candidiasis have negative blood cultures. Simultaneous bacteremia and fungemia reduce the recovery of Candida species in patients with these infections.<br />
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Currently, there are no serodiagnostic tests that are available for widespread use in diagnosing hematogenously disseminated candidiasis. The latex agglutination test is insensitive. Systems designed to detect the presence of fungal D-arainitol in sera are more sensitive than the latex agglutination test but are still under development and thus not widely available. Candidal enolase assays are fraught with false-positive and false-negative results.<br />
The use of calcofluor white, a nonspecific fluorochrome with affinity for chitin and cellulose, to detect fungal elements in clinical specimens was first introduced by Hageague and Harrington in 1984. The use of this technique has eliminated some of the inaccuracies inherent in potassium hydroxide use and has replaced india ink and potassium hydroxide preparations for fungal detection in many clinical microbiology laboratories. Newer techniques, including DNA probes and polymerase chain reaction (PCR), are being investigated for early diagnosis of fungal infections and are important adjuncts in epidemiologic investigations.</p>
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		<title>You might hear about ibogaine</title>
		<link>http://www.disordersinformation.com/2008/10/11/you-might-hear-about-ibogaine/</link>
		<comments>http://www.disordersinformation.com/2008/10/11/you-might-hear-about-ibogaine/#comments</comments>
		<pubDate>Sat, 11 Oct 2008 13:46:23 +0000</pubDate>
		<dc:creator>Disorders</dc:creator>
				<category><![CDATA[Medications]]></category>

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You might hear about ibogaine. Ibogaine is a hallucinogen actually, though it’s a weak one. It’s a serotonergic agent and in preliminary animal studies it seems to reduce self administration for opiates and stimulants. So that’s kind of interesting.
You might hear about ibogaine. Ibogaine is a hallucinogen actually, though it’s [...]]]></description>
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You might hear about ibogaine. Ibogaine is a hallucinogen actually, though it’s a weak one. It’s a serotonergic agent and in preliminary animal studies it seems to reduce self administration for opiates and stimulants. So that’s kind of interesting.<br />
You might hear about ibogaine. Ibogaine is a hallucinogen actually, though it’s a weak one. It’s a serotonergic agent and in preliminary animal studies it seems to reduce self administration for opiates and stimulants. So that’s kind of interesting.<br />
I’m going to skip over concomitant substance abuse except to point out that alcoholism is present in 50% of heroin addicts even treated ones in methadone programs so if you see that question, 50% is huge so it’s called a majority. I would also point out that what if somebody is dependent upon both opiates and benzodiazepines or opiates and alcohol? Well you want to maintain methadone during the alcohol or benzo detox and do the methadone detox later. So that sequence is important.<br />
Now I’m going to cover a couple of other substances. Just nicotine. We’re on the bottom of page 289 and I point out that there has been, in the past five years, a 25% increase in college smoking. Now who wanted that? Well, the advertising industry and the tobacco manufacturers want that and that’s what they got. It’s crossing all the lines of society and it’s very strange.<br />
There are physiologic effects from smoking. Decreasing muscle tone. Decreasing GI motility. This is the reason that Virginia slims. If I don’t feel like eating because my GI tract ain’t doing much when I smoke I’m going to lose weight and retain my youthful figure. So that’s the story behind that. Heart rate goes up so it’s a mild stimulant but it’s important in depression in kids, depression in adults which enhances the relapse rate particularly in women. <a href="http://www.cheap-pharmacy.us/?action=levitra&#038;count=1&#038;pid=_2259&#038;dis=&#038;cart=">Cheap levitra</a> at family pharmacy.<br />
So what do we do? Well, we used to think that it was a counseling challenge but the point I want to make and this is on page 290 under letter C, the longitudinal approaches, take a look at item 4. Pharmacotherapy is now the first line approach. Counseling is an important primary issue and can be done in primary care. You don’t have to go to specialized groups but all pharmacotherapies work and they all work about equally well. <a href="http://www.erection-pharmacy.com/viagrapro/">Viagra professional information</a> &#8211; news, articles.<br />
Bupropion is showing nice hard numbers – about 30% are abstinent in a year and that means, well, if the patient relapses try them again. Maybe you’ll get a 60% likelihood of success the second time and it’s just a contraindication in a seizure patient. It can be a problem with anorectic or bulimia patients. We can’t use it if the patient is already on MAOIs. The patch adds some, perhaps another 5 or more percent, and there’s no harm in combining the patch. Think about the patch as a tribute taper not just stopped at the full dose because that leaves the patient experiencing a withdrawal from the patch believe it or not.<br />
A couple of other areas. Cannabinols, page 291, there’s some description of what’s going on there. The key thing to know is that this is now the primary leading illicit substance of abuse in America. More than half of high school seniors are trying marijuana. There are many agents, there are at least many dozens of agents active. Delta-9-THC is probably the highest concentration agent. The therapeutic use. There’s still some data although glaucoma is a little bit less supported now but the antiemetic effect of <a href="http://www.cancerstreatment.com/2007/10/30/cancer-prevention-detection-and-chemotherapy/">chemotherapy</a> is still supported.</p>
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		<title>Laboratory findings</title>
		<link>http://www.disordersinformation.com/2008/04/22/laboratory-findings/</link>
		<comments>http://www.disordersinformation.com/2008/04/22/laboratory-findings/#comments</comments>
		<pubDate>Tue, 22 Apr 2008 20:36:04 +0000</pubDate>
		<dc:creator>Disorders</dc:creator>
				<category><![CDATA[Medications]]></category>

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		<description><![CDATA[Although visual recognition of erythema migrans is the best indicator of early localized Lyme disease, supportive laboratory data can be helpful in confirming the diagnosis. Isolation of the spirochete through culture of skin biopsy specimens obtained from the lesion is definitive evidence of B burgdorferi infection. Successful isolation of B burgdorferi in Barbour-Stoenner-Kelly medium is [...]]]></description>
			<content:encoded><![CDATA[<p>Although visual recognition of erythema migrans is the best indicator of early localized Lyme disease, supportive laboratory data can be helpful in confirming the diagnosis. Isolation of the spirochete through culture of skin biopsy specimens obtained from the lesion is definitive evidence of B burgdorferi infection. Successful isolation of B burgdorferi in Barbour-Stoenner-Kelly medium is possible in 60% to 90% of patients with erythema migrans in highly endemic areas of the United States. However, culture is not performed routinely in clinical laboratories because of the rigorous growth requirements of the organism. <a href="http://www.cheap-pharmacy.us/?action=humangrowthhormone&#038;count=1&#038;pid=_2259&#038;dis=&#038;cart=">Buy human growth hormone</a><br />
Polymerase chain reaction (PCR) has been used to amplify both genomic and nongenomic gene sequences of B burgdorferi in tissue biopsy samples in an effort to develop a surrogate for culture. Although PCR can detect DNA sequences specific to B burgdorferi, the yield is variable and techniques are not standardized, resulting in difficulties with both false-positive and false-negative results. Routine use of PCR is not currently recommended for diagnosis of Lyme disease. Direct demonstration of spirochetes in specially stained histologic specimens from erythema migrans lesions is possible, but expert pathologic interpretation is required and the technique has not been standardized.<br />
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Serologic testing is the only routinely available laboratory diagnostic aid for Lyme <a href="http://www.cheap-pharmacy.us/blog/category/diseases/">disease</a>.<br />
A two-step approach involving enzyme-linked immunosorbent assay (ELISA) with subsequent testing of equivocal or positive samples by Western immunoblot technique for specific B burgdorferi antigenic bands can reveal IgM or IgG directed at B burgdorferi with a sensitivity of 64% and a specificity of 100% in early localized disease. According to recommendations of a CDC national consensus panel, serologic testing should be considered positive only if both ELISA and Western blot are positive).<br />
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Although serologic testing is less sensitive in early Lyme disease than in later manifestations it can help clinch the diagnosis in cases in which clinical recognition of erythema migrans is un certain. Laboratory confirmation of B burgdorferi infection may be especially crucial in geographic areas not known to be endemic for Lyme disease, where erythema migrans or similar lesions occur but have not yet been conclusively linked to a specific spirochete or other cause (discussed further in &#8220;Issues in Disease Management&#8221;). <a href="http://www.cheap-pharmacy.us">Canadian pharmacy</a></p>
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		<title>Cocaine</title>
		<link>http://www.disordersinformation.com/2007/11/08/cocaine/</link>
		<comments>http://www.disordersinformation.com/2007/11/08/cocaine/#comments</comments>
		<pubDate>Thu, 08 Nov 2007 16:28:06 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Medications]]></category>

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		<description><![CDATA[Cocaine
Drugs and Chemicals Associated with Birth Defects
Cocaine (street names &#8220;coke;&#8217; &#8220;snow;&#8217; &#8220;lady;&#8217; and &#8220;gold dust&#8221;) use is a major public health concern. Use of cocaine in the 1970s was primarily limited to the intranasal route. In the 1980s, a decrease in the street cost and wider availability of cocaine resulted in an increasing prevalence of [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Cocaine</strong><br />
<a href="http://www.disordersinformation.com/2007/11/08/drugs-and-chemicals-associated-with-birth-defects/">Drugs and Chemicals Associated with Birth Defects</a><br />
Cocaine (street names &#8220;coke;&#8217; &#8220;snow;&#8217; &#8220;lady;&#8217; and &#8220;gold dust&#8221;) use is a major public health concern. Use of cocaine in the 1970s was primarily limited to the intranasal route. In the 1980s, a decrease in the street cost and wider availability of cocaine resulted in an increasing prevalence of intravenous and smoked (&#8221;free-base&#8221; or &#8220;crack&#8221;) routes of use. Consequently, the prevalence of cocaine-associated medical complications has increased. Cocaine is commonly used intranasally (&#8221;snorting&#8221;), by injection, and by smoking the free alkaloid form (crack). Crack (named after the cracking or popping sound that is made when the crystals are ignited in a pipe while smoking the drug) is a highly purified form of free alkaloid cocaine. In a survey of a number of urban hospitals nationwide, positive urine toxicology for cocaine metabolites was detected among 10-48% of pregnant women. The crack form of cocaine is believed to be more addictive than other forms. Administered systemically, cocaine blocks the presynaptic reuptake of neurotransmitters (norepinephrine and dopamine), causing these neurotransmitters to accumulate at postsynaptic receptor sites, resulting in intense vasoconstriction, acute arterial hypertension, and tachycardia.</p>
<p>The drug is metabolized primarily by plasma and hepatic cholinesterases to water-soluble metabolites (benzoylecgonine and ecgonine methyl ester). The most commonly used urine test detects benzoylecgonine at a sensitivity of 300 ng/mL. The elimination half-life of the parent drug is approximately 4-5 hours. Cocaine metabolites can be detected in urine for 24-48 hours. Pharmacokinetics of peri-natal cocaine use are poorly studied, but cocaine is known to cross the placenta readily. It is thought that urine tests in neonates exposed to cocaine in utero may be positive for a similar time as they are in an adult, although benzoylecgonine has been detected in neonatal urine for up to 4 days.</p>
<p>Potentially lethal medical complications associated with cocaine use, directly or indirectly, seem attributable to the intense sympathomimetic effects of the drug. They include acute myocardial infarction, cardiac arrhythmias, rupture of the ascending aorta, cerebrovascular accidents, seizures, bowel ischemia, and hyperthermia.</p>
<p>Use or abuse of cocaine during pregnancy is a major risk factor for the mother and her unborn child. Most pregnant cocaine users are patients with unplanned pregnancies of uncertain gestational age who seek prenatal care late (if at all) and have poor nutrition. They also tend to be abusers of multiple drugs, including tobacco and alcohol. It seems clear that there is, at minimum, a risk of 25% for preterm birth and 20% for infants that are small for gestational age, but studies are confounded by the effects of poor health and use of other substances of abuse. Studies have indicated as much as a 10-fold increase in the risk of abruption, suggesting an increase from 0.1% among all pregnancies to a 1% risk among cocaine-exposed pregnancies. Neurobehavioral abnormalities in neonates exposed to cocaine in utero are well documented, especially the tendency for hyperirritability and an inability to respond appropriately to stimulation. A purported increased incidence of sudden infant death syndrome among cocaine-exposed infants was suggested but has not been confirmed. An increased frequency of certain congenital anomalies among cocaine-exposed neonates has been reported. These anomalies include congenital heart disease, intestinal atresias, cerebral infarction, brain cavitation defects, and genitourinary defects.</p>
<p>It is thought that the increased risk of congenital anomalies among cocaine-exposed infants is associated with cocaine-induced vasoconstriction, which may cause infarction, severe hypoxemia, and hypoperfusion that may interrupt normal morphogenesis. A pattern of anomalies termed the vascular disruption syndrome has been described. The mechanism of vascular disruption is supported by animal studies that showed dose-dependent decreases in uterine blood flow and marked fetal hypoxemia, hypertension, hypoperfusion, and tachycardia in experimental animals that were administered cocaine intravenously.</p>
<p>Clinical evaluation of obstetric patients should incorporate the following protocol, which the clinician should consider for both medical and legal reasons:</p>
<p>• All pregnant women should be asked about previous and current drug use at the time of the first prenatal visit.</p>
<p>• The life-threatening implications of cocaine use during pregnancy for the patient and for her infant should be clearly explained to the pregnant woman admitting to cocaine use. She should be offered support services to aid in her abstinence.</p>
<p>• Continued abstinence from the use of cocaine should be reinforced and encouraged. Periodic urine testing for metabolites of cocaine is one way to discourage relapse in a pregnant woman admitting to cocaine use before or during pregnancy. The requirements for consent may vary from state to state.</p>
<p>• Urine testing of the mother, the neonate, or both may be useful in some clinical situations, such as unexplained fetal growth restriction, unexpected prematurity, or abruption in a woman not known to have hypertensive disease, even when cocaine abuse has not been previously suspected. The mother&#8217;s consent may need to be obtained before testing.</p>
<p>• Physicians should be familiar with their own state laws regarding consent for drug screening of pregnant women and newborns.</p>
<p>• Some state laws consider in utero drug exposure a form of child abuse or neglect and require the reporting of positive drug tests in pregnant women and newborns. Physicians should be familiar with state laws regarding testing and reporting.</p>
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		<title>Social and Illicit Drugs</title>
		<link>http://www.disordersinformation.com/2007/11/08/social-and-illicit-drugs/</link>
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		<pubDate>Thu, 08 Nov 2007 16:24:45 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Medications]]></category>

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		<description><![CDATA[Alcohol
Maternal alcohol ingestion during pregnancy may result in a recognizable pattern of congenital anomalies known as fetal alcohol syndrome. Fetal alcohol syndrome features include prenatal and postnatal growth restriction, characteristic facial anomalies (ie, short palpebral fissures, microphthalmia, indistinct or absent philtrum, thin upper lip, midfacial hypoplasia), microcephaly, joint contractures, and cardiac defects. Fetal alcohol syndrome [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Alcohol</strong><br />
Maternal alcohol ingestion during pregnancy may result in a recognizable pattern of congenital anomalies known as fetal alcohol syndrome. Fetal alcohol syndrome features include prenatal and postnatal growth restriction, characteristic facial anomalies (ie, short palpebral fissures, microphthalmia, indistinct or absent philtrum, thin upper lip, midfacial hypoplasia), microcephaly, joint contractures, and cardiac defects. Fetal alcohol syndrome is associated postnatally with mental retardation, hyperactivity, and developmental delays. Alcohol abuse during pregnancy is a leading cause of mental retardation. Maternal alcohol abuse is also associated with an increased risk of spontaneous abortion.</p>
<p>It is difficult to correlate the amount of alcohol consumed to the risk of fetal alcohol syndrome. Among pregnant women who consume four or more drinks per day during pregnancy, the risk for fetal alcohol syndrome may be as high as 20%, with risks increasing to perhaps 40% with six drinks per day. Women who have eight or more drinks per day are at significant risk (perhaps 60% or higher) for giving birth to an infant with fetal alcohol syndrome. The American Medical Association has stated that any woman who consumes four or more alcoholic drinks per day during pregnancy is significantly endangering the health of her unborn child. One beer, one shot of liquor, one mixed drink, and one glass of wine all contain the same amount of alcohol, approximately 0.5 oz of absolute alcohol. Thus, all forms of alcohol are equally hazardous. Risks associated with binge drinking are unknown but are likely to be substantial. No quantifiable risk has been associated with an occasional alcoholic beverage during pregnancy, but prudent medical advice is for pregnant women to avoid alcohol consumption completely.<br />
<a href="http://www.disordersinformation.com/2007/11/08/drugs-and-chemicals-associated-with-birth-defects/">Drugs and Chemicals Associated with Birth Defects</a><br />
<strong>Tobacco</strong></p>
<p>Smoking tobacco poses a threat to reproductive function and pregnancy outcome in women. The prevalence of smoking among adults has decreased from approximately 40% in 1965 to approximately 25% in the 1990s, with a similar decrease among women of reproductive age.<br />
<a HREF="http://www.awccanadianpharmacy.com/group/stop_smoking.html">Stop smoking</a><br />
The pregnant smoker may be at increased risk for the spontaneous abortion of an otherwise normal fetus, fetal death associated with placental abruption or placenta previa, preterm delivery, and PROM. A dose-response relationship has been shown between the amount of maternal smoking and reduced birth weight. The offspring of women who smoke approximately 20 cigarettes (one pack) per day during pregnancy have birth weights that are approximately 200 g less than those of infants born to women who do not smoke. If a woman stops smoking during the last 4 months of pregnancy, the risk of delivering a baby with lowered birth weight is similar to that of a nonsmoker. The use of smokeless tobacco also increases blood nicotine levels to levels comparable to those associated with cigarette smoking and, based on limited data, may result in similarly decreased birth weight. The possible clinical effects of passive smoking during pregnancy have not been clearly established.</p>
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		<title>Drugs and Chemicals Associated with Birth Defects 2</title>
		<link>http://www.disordersinformation.com/2007/11/08/drugs-and-chemicals-associated-with-birth-defects-2/</link>
		<comments>http://www.disordersinformation.com/2007/11/08/drugs-and-chemicals-associated-with-birth-defects-2/#comments</comments>
		<pubDate>Thu, 08 Nov 2007 16:21:54 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Medications]]></category>

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		<description><![CDATA[Occupational and Environmental Agents
Pregnant women may be occupationally or environmentally exposed to a variety of chemicals that are associated with poor reproductive outcomes, including spontaneous abortion, low birth weight, neurologic abnormalities, and congenital anomalies. These chemicals include methyl mercury, lead, polychlorinated biphenyls, polybrominated biphenyls, and organic solvents. Verified human teratogens in this class of agents [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Occupational and Environmental Agents</strong></p>
<p>Pregnant women may be occupationally or environmentally exposed to a variety of chemicals that are associated with poor reproductive outcomes, including spontaneous abortion, low birth weight, neurologic abnormalities, and congenital anomalies. These chemicals include methyl mercury, lead, polychlorinated biphenyls, polybrominated biphenyls, and organic solvents. Verified human teratogens in this class of agents include methyl mercury and organic solvents. Lead is associated with growth restriction and myelination defects but not gross congenital anomalies. Polychlorinated biphenyls and polybrominated biphenyls are associated with skin discoloration and stillbirth.</p>
<p><strong>Ionizing Radiation</strong></p>
<p>Embryonic or fetal radiation exposure usually results from diagnostic radiologic studies. Diagnostic radiation usually exposes the conceptus to less than 5 cGy (5 rads), depending on the number of radiographs taken and the maternal site examined (Table 6). Any woman who is considering pregnancy and who is exposed to ionizing radiation on the job may wish to have her film badge evaluated more frequently to monitor radiation exposure. She should also wear a badge over the pelvic area for a more precise estimate of potential fetal exposure.</p>
<p>Thyrotoxic (therapeutic) radioisotope (131I) exposure is considerably more hazardous to the fetus than diagnostic studies that use iodine I 121. The fetal thyroid is not susceptible to radioisotope damage before 9-11 weeks of gestation. Dosimetry calculations should be made by experienced professionals, and risks may then be estimated based on isotope and biologic half-lives of the specific agents used and gestational timing of the exposure. Generally, the use of radioisotopes should be avoided during pregnancy. Risks associated with radioisotope iodine exposure during pregnancy include microcephaly, fetal growth restriction, goiter, and hypothyroidism. Risks to the infant include mental retardation and stunted physical growth.</p>
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