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	<title>Cardiophile MD Archive &#187; Multiple Choice Questions</title>
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	<link>http://www.cardiophile.net</link>
	<description>Archive of Cardiophile MD</description>
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		<title>Smoker&#8217;s paradox</title>
		<link>http://www.cardiophile.net/2010/06/smokers-paradox.html</link>
		<comments>http://www.cardiophile.net/2010/06/smokers-paradox.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:21:43 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5641</guid>
		<description><![CDATA[All of the following are true of &#8220;smoker&#8217;s paradox&#8221; except: A. It is a beneficial effect of smoking B. Better outcome following reperfusion strategies C. Likely to undergo reperfusion strategies at a younger age D. Lower co-morbidity Answer: A. It is a beneficial effect of smoking Braunwald&#8217;s heart diseases, 8th Edition, Chapter 39, Page 1004.]]></description>
			<content:encoded><![CDATA[<p>All of the following are true of &#8220;smoker&#8217;s paradox&#8221; except:</p>
<p>A. It is a beneficial effect of smoking</p>
<p>B. Better outcome following reperfusion strategies</p>
<p>C. Likely to undergo reperfusion strategies at a younger age</p>
<p>D. Lower co-morbidity</p>
<p><strong>Answer: </strong>A. It is a beneficial effect of smoking</p>
<p>Braunwald&#8217;s heart diseases, 8th Edition, Chapter 39, Page 1004.</p>
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		<title>Nitric oxide synthase</title>
		<link>http://www.cardiophile.net/2010/06/nitric-oxide-synthase.html</link>
		<comments>http://www.cardiophile.net/2010/06/nitric-oxide-synthase.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:20:02 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5639</guid>
		<description><![CDATA[Endothelial nitric oxide synthase is: A. Type I B. Type II C. Type III D. Type IV Answer: C. Type III Endothelial nitric oxide synthase (eNOS) is Type III. The other types are brain or neuronal NOS (b or nNOS, type I) and inducible NOS (iNOS, type II). All NOS isoforms contain domains for binding [...]]]></description>
			<content:encoded><![CDATA[<p>Endothelial nitric oxide synthase is:</p>
<p>A. Type I</p>
<p>B. Type II</p>
<p>C. Type III</p>
<p>D. Type IV</p>
<p><strong>Answer: </strong>C. Type III</p>
<p>Endothelial nitric oxide synthase (eNOS) is Type III. The other types are brain or neuronal NOS (b or nNOS, type I) and inducible NOS (iNOS, type II). All NOS isoforms contain domains for binding calmodulin, nicotinamide adenine dinucleotide phosphate (NADPH), flavin adenine dinucleotide (FAD), and flavin mononucleotide (FMN). NOS catalyzes the oxidation of L-arginine to produce L-citrulline and nitric oxide (NO).</p>
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		<title>Myocardial postconditioning</title>
		<link>http://www.cardiophile.net/2010/06/myocardial-postconditioning-2.html</link>
		<comments>http://www.cardiophile.net/2010/06/myocardial-postconditioning-2.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:18:36 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5637</guid>
		<description><![CDATA[Pathways involved in myocardial postconditioning include all of the following except: A. Reperfusion injury salvage kinase (RISK) pathway B. MEK1/2-ERK pathway C. PI3K-Akt pathway D. GMP Shunt pathway Answer: D. GMP Shunt pathway Ischemic postconditioning, was initially described as a 44% reduction in infarct size with three cycles of 30 second occlusion &#8211; re-occlusion during [...]]]></description>
			<content:encoded><![CDATA[<p>Pathways involved in myocardial postconditioning include all of the following except:</p>
<p>A. Reperfusion injury salvage kinase (RISK) pathway</p>
<p>B. MEK1/2-ERK pathway</p>
<p>C. PI3K-Akt pathway</p>
<p>D. GMP Shunt pathway</p>
<p><strong>Answer: </strong>D. GMP Shunt pathway</p>
<p>Ischemic postconditioning, was initially described as a 44% reduction in infarct size with three cycles of 30 second occlusion &#8211; re-occlusion during reperfusion after a 60 minute occlusion of left anterior descending coronary artery in a dog model. The mechanism proposed is the upregulation of prosurvival kinases termed the reperfusion injury salvage kinase (RISK) pathway.  PI3K-Akt and MEK 1/2-p42/44 kinases are important components of this cell survival pathway. These have anti-apoptotic effects.</p>
<p>Tsang A et al,Myocardial postconditioning: reperfusion injury revisited. Am J Physiol Heart Circ Physiol 289: H2-H7, 2005</p>
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		<title>Lithium and valvular disease in offspring</title>
		<link>http://www.cardiophile.net/2010/06/lithium-and-valvular-disease-in-offspring.html</link>
		<comments>http://www.cardiophile.net/2010/06/lithium-and-valvular-disease-in-offspring.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:17:06 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5635</guid>
		<description><![CDATA[Maternal intake of lithium during pregnancy is associated with: A. Tricupsid valve disease B. Mitral valve disease C. Aortic valve disease D. Pulmonary valve disease Answer: A. Tricupsid valve disease Maternal intake of lithium during pregnancy has been associated with Ebstein&#8217;s anomaly of tricuspid valve.]]></description>
			<content:encoded><![CDATA[<p>Maternal intake of lithium during pregnancy is associated with:</p>
<p>A. Tricupsid valve disease</p>
<p>B. Mitral valve disease</p>
<p>C. Aortic valve disease</p>
<p>D. Pulmonary valve disease</p>
<p><strong>Answer: </strong>A. Tricupsid valve disease</p>
<p>Maternal intake of lithium during pregnancy has been associated with Ebstein&#8217;s anomaly of tricuspid valve.</p>
]]></content:encoded>
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		<title>Endothelin</title>
		<link>http://www.cardiophile.net/2010/06/endothelin.html</link>
		<comments>http://www.cardiophile.net/2010/06/endothelin.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:15:34 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5633</guid>
		<description><![CDATA[Vasoconstriction by endothelin is mediated by: A. Activation of protein kinase C in vascular smooth muscle B. Prostacyclin activation in vascular smooth muscle C. Synthesis of EDHF in vascular endothelium D. Acetyl choline mediated vasoconstriction Answer: A. Activation of protein kinase C in vascular smooth muscle Endothelins (ET-1, ET-2 and ET-3) are peptide endothelium dependent [...]]]></description>
			<content:encoded><![CDATA[<p>Vasoconstriction by endothelin is mediated by:</p>
<p>A. Activation of protein kinase C in vascular smooth muscle</p>
<p>B. Prostacyclin activation in vascular smooth muscle</p>
<p>C. Synthesis of EDHF in vascular endothelium</p>
<p>D. Acetyl choline mediated vasoconstriction</p>
<p><strong>Answer: </strong>A. Activation of protein kinase C in vascular smooth muscle</p>
<p>Endothelins (ET-1, ET-2 and ET-3) are peptide endothelium dependent constricting factors. ET-1 is a potent vasoconstrictor and is formed from the precursor pre-pro-endothelin by endothelin converting enzyme. ET-A and ET-B receptors are present,of which ET-A receptor mediates vasoconstiction by activation of protein kinase C in vascular smooth muscle. ET-B mediated vasoconstriction is partially offset by ET-B mediated eNOS activity.</p>
]]></content:encoded>
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		<item>
		<title>Endothelial cell antithrombotic mechanisms</title>
		<link>http://www.cardiophile.net/2010/06/endothelial-cell-antithrombotic-mechanisms.html</link>
		<comments>http://www.cardiophile.net/2010/06/endothelial-cell-antithrombotic-mechanisms.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:13:32 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5630</guid>
		<description><![CDATA[All of the following molecules are involved in the antithrombotic mechanisms of the endothelial cell except: A. Heparan sulphate B. Thrombomodulin C. t-PA D. Lipoprotein (a) Answer: D. Lipoprotein (a) Heparan sulfate proteoglycan molecules on the surface of the endothelial cell act as a co-factor for antithrombin III. Thrombomodulin binds thrombin molecules and exerts antithrombotic [...]]]></description>
			<content:encoded><![CDATA[<p>All of the following molecules are involved in the antithrombotic mechanisms of the endothelial cell except:</p>
<p>A. Heparan sulphate</p>
<p>B. Thrombomodulin</p>
<p>C. t-PA</p>
<p>D. Lipoprotein (a)</p>
<p><strong>Answer: </strong>D. Lipoprotein (a)</p>
<p>Heparan sulfate proteoglycan molecules on the surface of the endothelial cell act as a co-factor for antithrombin III.<br />
Thrombomodulin binds thrombin molecules and exerts antithrombotic properties by activating proteins S and C. Tissue type plasminogen activator produced by endothelial cells can lyse thrombi as soon as they start forming. Lipoprotein (a) on the other hand promotes ahterothrombosis.</p>
]]></content:encoded>
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		<item>
		<title>EDHF</title>
		<link>http://www.cardiophile.net/2010/06/edhf.html</link>
		<comments>http://www.cardiophile.net/2010/06/edhf.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:11:22 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5628</guid>
		<description><![CDATA[All of the following are true of endothelium dependent hyperpolarizing factor (EDHF) except: A. Hyperpolarizes vascular smooth muscle B. Acts via nitric oxide C. Metabolite of arachidonic acid D. Produced by cytochrome P-450 epoxygenase pathway Answer: B. Acts via nitric oxide Endothelium-dependent hyperpolarizing factor (EDHF) hyperpolarizes vascular smooth muscle and dilates arteries by opening calcium-activated [...]]]></description>
			<content:encoded><![CDATA[<p>All of the following are true of endothelium dependent hyperpolarizing factor (EDHF) except:</p>
<p>A. Hyperpolarizes vascular smooth muscle</p>
<p>B. Acts via nitric oxide</p>
<p>C. Metabolite of arachidonic acid</p>
<p>D. Produced by cytochrome P-450 epoxygenase pathway</p>
<p><strong>Answer: </strong>B. Acts via nitric oxide</p>
<p>Endothelium-dependent hyperpolarizing factor (EDHF) hyperpolarizes vascular smooth muscle and dilates arteries by opening calcium-activated potassium channels. The exact biochemical nature of EDHF is to be determined. The possible candidates are epoxyeicosatienoic acid and endothelium-derived hydrogen peroxide.</p>
]]></content:encoded>
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		<title>Determinants of myocardial oxygen consumption</title>
		<link>http://www.cardiophile.net/2010/06/determinants-of-myocardial-oxygen-consumption.html</link>
		<comments>http://www.cardiophile.net/2010/06/determinants-of-myocardial-oxygen-consumption.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:09:00 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5626</guid>
		<description><![CDATA[All of the following are determinants of myocardial oxygen consumption except: A. Systolic pressure B. Diastolic pressure C. Heart rate D. Left ventricular contractility Answer: B. Diastolic pressure The major determinants of myocardial oxygen consumption are heart rate, systolic pressure and left ventricular contractility. The product of systolic pressure and heart rate is known as [...]]]></description>
			<content:encoded><![CDATA[<p>All of the following are determinants of myocardial oxygen consumption except:</p>
<p>A. Systolic pressure</p>
<p>B. Diastolic pressure</p>
<p>C. Heart rate</p>
<p>D. Left ventricular contractility</p>
<p><strong>Answer: </strong>B. Diastolic pressure</p>
<p>The major determinants of myocardial oxygen consumption are heart rate, systolic pressure and left ventricular contractility. The product of systolic pressure and heart rate is known as double product. The product of double product and left ventricular ejection time is sometimes called the triple product. The double product is a commonly measured indicator of myocardial oxygen consumption. The summary report of the treadmill exercise test displays the double product in each stage.</p>
]]></content:encoded>
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		<item>
		<title>Delayed preconditioning</title>
		<link>http://www.cardiophile.net/2010/06/delayed-preconditioning.html</link>
		<comments>http://www.cardiophile.net/2010/06/delayed-preconditioning.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:06:21 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5624</guid>
		<description><![CDATA[Mechanisms of chronic preconditioning include all the following except: A. Downregulation of iNOS B. Upregulation of COX-2 C. Opening of mitochondrial K+ATP channels D. Involves protein synthesis Answer: A. Downregulation of iNOS Chronic or delayed preconditioning involves protein synthesis with upregulation of iNOS (inducible nitric oxide synthase), cyclooxygenase (COX-2) and opening of mitochondrial K+ATP channels. [...]]]></description>
			<content:encoded><![CDATA[<p>Mechanisms of chronic preconditioning include all the following except:</p>
<p>A. Downregulation of iNOS</p>
<p>B. Upregulation of COX-2</p>
<p>C. Opening of mitochondrial K+ATP channels</p>
<p>D. Involves protein synthesis</p>
<p><strong>Answer: </strong>A. Downregulation of iNOS</p>
<p>Chronic or delayed preconditioning involves protein synthesis with upregulation of iNOS (inducible nitric oxide synthase), cyclooxygenase (COX-2) and opening of mitochondrial K+ATP channels. It can persist up to 4 days.</p>
]]></content:encoded>
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		<item>
		<title>Coronary vascular resistance</title>
		<link>http://www.cardiophile.net/2010/06/coronary-vascular-resistance.html</link>
		<comments>http://www.cardiophile.net/2010/06/coronary-vascular-resistance.html#comments</comments>
		<pubDate>Thu, 10 Jun 2010 07:04:21 +0000</pubDate>
		<dc:creator>Johnson Francis</dc:creator>
				<category><![CDATA[Multiple Choice Questions]]></category>

		<guid isPermaLink="false">http://www.cardiophile.net/?p=5622</guid>
		<description><![CDATA[Extravascular compressive component of coronary vascular resistance is: A. R1 B. R2 C. R3 D. R4 Answer: C. R3 R1 is the epicardial conduit resistance, which is negligible unless the obstruction is more than 50% of luminal diameter. R2 is the microcirculatory resistance in the small arteries and arterioles. R3 is compressive resistance and is [...]]]></description>
			<content:encoded><![CDATA[<p>Extravascular compressive component of coronary vascular resistance is:</p>
<p>A. R1</p>
<p>B. R2</p>
<p>C. R3</p>
<p>D. R4</p>
<p><strong>Answer: </strong>C. R3</p>
<p>R1 is the epicardial conduit resistance, which is negligible unless the obstruction is more than 50% of luminal diameter. R2 is the microcirculatory resistance in the small arteries and arterioles. R3 is compressive resistance and is related to the cardiac contraction and the systolic pressure developed in the left ventricle.</p>
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