{"id":46664,"date":"2021-07-04T05:44:53","date_gmt":"2021-07-04T00:14:53","guid":{"rendered":"https:\/\/johnsonfrancis.org\/professional\/?p=46664"},"modified":"2021-07-04T05:44:53","modified_gmt":"2021-07-04T00:14:53","slug":"cardiology-mcqs-2","status":"publish","type":"post","link":"https:\/\/johnsonfrancis.org\/professional\/cardiology-mcqs-2\/","title":{"rendered":"Cardiology MCQs"},"content":{"rendered":"<p><iframe loading=\"lazy\" width=\"560\" height=\"315\" src=\"https:\/\/www.youtube.com\/embed\/-Y7HcJO_GVQ\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"><\/iframe><\/p>\n<h2><span style=\"color: #008000;\">Cardiology MCQs<\/span><\/h2>\n<p><span style=\"color: #0000ff;\"><strong>Which of the following is NOT a drug used for metabolic modulation in heart failure?<\/strong><\/span><\/p>\n<ol>\n<li>Trimetazidine<\/li>\n<li>Ranolazine<\/li>\n<li>Perhexiline<\/li>\n<li>Sacubitril-valsartan<\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 4. Sacubitril-valsartan<\/strong><\/span><\/p>\n<p>Sacubitril-valsartan is an angiotensin receptor-neprilysin inhibitor (ARNI). Trimetazidine is a 3-ketoacyl coenzyme A thiolase inhibitor, while ranolazine inhibits the late sodium current. Perhexiline inhibits carnitine palmitoyl transferase. Latter three are metabolic modulators while sacubitril-valsartan is a hemodynamic modulator in heart failure [Ashrafian H, Neubauer S. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/21258118\/\">Metabolic modulation in heart failure: high time for a definitive clinical trial<\/a>. Heart. 2011 Feb;97(4):267-8].<\/p>\n<p><span style=\"color: #0000ff;\"><strong>Fleischner\u2019s sign is:<\/strong><\/span><\/p>\n<ol>\n<li>Prominent central pulmonary artery in acute massive pulmonary embolism<\/li>\n<li>Partial anomalous pulmonary venous drainage to inferior vena cava<\/li>\n<li>Supracardiac shadow in total anomalous pulmonary venous drainage<\/li>\n<li>None of the above<\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 1. Prominent central pulmonary artery in acute massive pulmonary embolism<\/strong><\/span><\/p>\n<p>[Cooksley T, Husein B, Iqbal J, Bright J. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/20656435\/\">Fleischner\u2019s sign in a massive pulmonary embolism<\/a>. J Emerg Med. 2012 Jun;42(6):698-9]. Partial anomalous pulmonary venous drainage to inferior vena cava seen on chest X-ray is scimitar sign. Supracardiac shadow in total anomalous pulmonary venous drainage is known as figure of 8 sign,&nbsp; cottage loaf sign and snow man appearance.<\/p>\n<p><span style=\"color: #0000ff;\"><strong>Biomarker useful in the evaluation of aortic dissection:<\/strong><\/span><\/p>\n<ol>\n<li>D-dimer<\/li>\n<li>Troponin<\/li>\n<li>Soluble ST2<\/li>\n<li>B-type natriuretic peptide<\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 1. D-dimer<\/strong><\/span><\/p>\n<p>Though several biomarkers have been evaluated in aortic dissection, only D-dimer is considered clinically feasible. It is markedly elevated in aortic dissection. Cut off value of 500 ng\/mL can be used to rule out aortic dissection with a negative likelihood ratio of 0.07 within the first 24 hours [Suzuki T, Distante A, Zizza A, Trimarchi S, Villani M, Salerno Uriarte JA, De Luca Tupputi Schinosa L, Renzulli A, Sabino F, Nowak R, Birkhahn R, Hollander JE, Counselman F, Vijayendran R, Bossone E, Eagle K; IRAD-Bio Investigators. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/19433758\/\">Diagnosis of acute aortic dissection by D-dimer: the International Registry of Acute Aortic Dissection Substudy on Biomarkers (IRAD-Bio) experience<\/a>. Circulation. 2009 May 26;119(20):2702-7]. Those with younger age, thrombosed false lumen without ulcer like projections and shorter dissection length were likely to have false negative D-dimer values [Hazui H, Nishimoto M, Hoshiga M, Negoro N, Muraoka H, Murai M, Ohishi Y, Fukumoto H, Morita H. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17127806\/\">Young adult patients with short dissection length and thrombosed false lumen without ulcer-like projections are liable to have false-negative results of D-dimer testing for acute aortic dissection based on a study of 113 cases<\/a>. Circ J. 2006 Dec;70(12):1598-601]. Soluble ST2 and B-type natriuretic peptide are biomarkers for heart failure.<\/p>\n<p><span style=\"color: #0000ff;\"><strong>Wrong statement about neoatherosclerosis:<\/strong><\/span><\/p>\n<ol>\n<li>Caused by chronic inflammation in neointimal proliferation within a coronary stent<\/li>\n<li>Disruption of neoatheroma can cause thrombotic occlusion<\/li>\n<li>Lower prevalence in drug eluting stents<\/li>\n<li>Occurs earlier in drug eluting stents<\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 3. Lower prevalence in drug eluting stents<\/strong><\/span><\/p>\n<p>Neoatherosclerosis was noted in 31% of drug eluting stent lesions and 16% of bare metal stent lesions in the CVPath stent registry of 406 neoatherosclerotic lesions from 299 autopsies [Nakazawa G, Otsuka F, Nakano M, Vorpahl M, Yazdani SK, Ladich E, Kolodgie FD, Finn AV, Virmani R. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/21376502\/\">The pathology of neoatherosclerosis in human coronary implants bare-metal and drug-eluting stents<\/a>. J Am Coll Cardiol. 2011 Mar 15;57(11):1314-22]. Mean implant duration was 1.5 years in drug eluting stents and 6.1 years in bare metal stents in that study.<\/p>\n<p><span style=\"color: #0000ff;\"><strong>Adverse health effects of partially hydrogenated vegetable oils are thought to be due to:<\/strong><\/span><\/p>\n<ol>\n<li>Trans fatty acids<\/li>\n<li>Mono unsaturated fatty acids<\/li>\n<li>Poly unsaturated fatty acids<\/li>\n<li>Saturated fatty acids<\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 1. Trans fatty acids<\/strong><\/span><\/p>\n<p>Trans fatty acids cause inflammation and calcification of arterial walls. They also inhibit cyclooxygenase needed for conversion of arachidonic acid to prostacyclin, a compound beneficial for the vascular tree. Total trans fat intake was associated with all cause mortality (34% increase), coronary heart disease mortality (28% increase) and total coronary heart disease (21% increase) in a meta analysis [de Souza RJ, Mente A, Maroleanu A, Cozma AI, Ha V, Kishibe T, Uleryk E, Budylowski P, Sch\u00fcnemann H, Beyene J, Anand SS. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/26268692\/\">Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies<\/a>. BMJ. 2015 Aug 11;351:h3978].<\/p>\n<p><span style=\"color: #0000ff;\"><strong>Wrong statement about fetal circulation:<\/strong><\/span><\/p>\n<ol>\n<li>Ductus venosus has a higher oxygen saturation than left atrium<\/li>\n<li>Eustachian valve directs inferior vena caval blood to the right ventricle<\/li>\n<li>Only 12% of the blood ejected from the right ventricle reaches the lungs<\/li>\n<li>45% of the combined ventricular output is delivered to the placenta<\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 2. Eustachian valve directs inferior vena caval blood to the right ventricle<\/strong><\/span><\/p>\n<p>Eustachian valve directs inferior vena caval blood across the patent foramen ovale into the left atrium. Saturation of blood in ductus venosus is 80-90% while that in the left atrium is only 65% saturated in the fetus. This is because the lungs are not functional in the fetus. Blood in the ductus venosus is that from the umbilical vein returning after oxygenation from the placenta [John PJ. <a href=\"https:\/\/academic.oup.com\/bjaed\/article\/5\/4\/107\/475171\">The fetal circulation<\/a>. Contin Educ Anaesth Crit Care Pain. 2005;5(4):107:112].<\/p>\n<p><strong><span style=\"color: #0000ff;\">In cyanotic congenital heart disease, sum of the diameters of pulmonary arteries divided by the diameter of the aorta is known as:<\/span><\/strong><\/p>\n<ol>\n<li>Nakata index<\/li>\n<li>McGoon ratio<\/li>\n<li>Wilkins score<\/li>\n<li>None of the above<\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 2. McGoon ratio<\/strong><\/span><\/p>\n<p>Two important measures on the size of pulmonary arteries are the McGoon ratio and the Nakata index. Nakata index is the sum of the cross-sectional area of the pulmonary arteries divided by the body surface area. Nakata index was initially described as pulmonary artery or PA index by Nakata S et al [Nakata S, Imai Y, Takanashi Y, Kurosawa H, Tezuka K, Nakazawa M, Ando M, Takao A. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/6482493\/\">A new method for the quantitative standardization of cross-sectional areas of the pulmonary arteries in congenital heart diseases with decreased pulmonary blood flow<\/a>. J Thorac Cardiovasc Surg. 1984 Oct;88(4):610-9]. These indices are useful in predicting likelihood of successful single stage repair. Wilkins echocardiographic score is for the assessment of mitral valve suitability for balloon mitral valvotomy in mitral stenosis.<\/p>\n<p><strong><span style=\"color: #0000ff;\">Wrong statement about left ventricular non compaction:<\/span><\/strong><\/p>\n<ol>\n<li>Characterized by shallow trabeculations<\/li>\n<li>Most involved region is the apex<\/li>\n<li>Genetic transmission in 30-50%<\/li>\n<li>NOTCH pathway is affected<\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 1. Characterized by shallow trabeculations<\/strong><\/span><\/p>\n<p>Non-compaction of left ventricle is often classified as a cardiomyopathy and is characterized by abnormal deep trabeculations, which is more at the apex [Towbin JA, Lorts A, Jefferies JL. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/25865865\/\">Left ventricular non-compaction cardiomyopathy<\/a>. Lancet. 2015 Aug 22;386(9995):813-25.]. It was thought that embryological arrest of normal endomyocardial morphogenesis was the cause of non-compaction. But some authors have disputed this theory [D\u2019Silva A, Jensen B. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/33153995\/\">Left ventricular non-compaction cardiomyopathy: how many needles in the haystack?<\/a> Heart. 2020 Nov 5:heartjnl-2020-316945].<\/p>\n<p><strong><span style=\"color: #0000ff;\">Important J wave syndromes are Early Repolarization Syndrome and Brugada syndrome. J wave is mediated by:<\/span><\/strong><\/p>\n<ol>\n<li>Transient outward potassium current I<sub>to<\/sub><\/li>\n<li>Slow component of delayed rectifier potassium current&nbsp;I<sub>Ks<\/sub><\/li>\n<li>Fast component of delayed rectifier potassium current&nbsp;I<sub>Kr<\/sub><\/li>\n<li>Inwardly rectifying potassium current&nbsp;I<sub>K1<\/sub><\/li>\n<\/ol>\n<p><span style=\"color: #008000;\"><strong>Correct answer: 1. <\/strong><strong>Transient outward potassium current I<sub>to<\/sub><\/strong><\/span><\/p>\n<p>J wave is mediated by the transient outward potassium current I<sub>to<\/sub>. It has been suggested that arrhythmias associated early repolarization, Brugada syndrome, hypothermia and those occurring in the acute phase of ST elevation myocardial infarction are linked to abnormalities in I<sub>to <\/sub>mediated J wave [Antzelevitch C, Yan GX. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/20153265\/\">J wave syndromes<\/a>. Heart Rhythm. 2010 Apr;7(4):549-58].<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Cardiology MCQs Which of the following is NOT a drug used for metabolic modulation in heart failure? Trimetazidine Ranolazine Perhexiline Sacubitril-valsartan Correct answer: 4. Sacubitril-valsartan Sacubitril-valsartan is an angiotensin receptor-neprilysin inhibitor (ARNI). Trimetazidine is a 3-ketoacyl coenzyme A thiolase inhibitor, while ranolazine inhibits the late sodium current. Perhexiline inhibits carnitine palmitoyl transferase. Latter three are [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":31007,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"nf_dc_page":"","footnotes":""},"categories":[3,5],"tags":[],"class_list":["post-46664","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-cardiology-mcq","category-dm-dnb-cardiology-entrance"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.9 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Cardiology MCQs - All About Cardiovascular System and Disorders<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/johnsonfrancis.org\/professional\/cardiology-mcqs-2\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Cardiology MCQs - All About Cardiovascular System and Disorders\" \/>\n<meta property=\"og:description\" content=\"Cardiology MCQs Which of the following is NOT a drug used for metabolic modulation in heart failure? 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