tag:blogger.com,1999:blog-8383794407502276712024-02-07T23:52:42.964-04:00MEDICAL BIOCHEMISTRY MADE EASYUnderstanding cellular metabolic process will help us to
understand the disease process when some metabolic
events go wrong!! With this blog I would like to share my
medical biochemistry knowledge with you!!!Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.comBlogger122125tag:blogger.com,1999:blog-838379440750227671.post-61057942942492162622018-03-18T06:36:00.003-04:002018-03-18T06:36:30.090-04:00Sample Question on Detoxification (Xenobiotics Metabolism)<iframe allowfullscreen="" frameborder="0" height="344" src="https://www.youtube.com/embed/XkfSJ64oThM" width="459"></iframe>Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com1tag:blogger.com,1999:blog-838379440750227671.post-82138449790760379022018-03-18T06:36:00.001-04:002018-03-18T06:36:28.883-04:00Sample Question on Detoxification (Xenobiotics Metabolism)<iframe allowfullscreen="" frameborder="0" height="344" src="https://www.youtube.com/embed/XkfSJ64oThM" width="459"></iframe>Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-4057382692624135062018-03-16T22:07:00.001-04:002018-03-16T22:07:46.854-04:00Sample Question on Lipoprotein Metabolism Up to 4K<iframe allowfullscreen="" frameborder="0" height="344" src="https://www.youtube.com/embed/0YbqaqbCdfQ" width="459"></iframe>Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-58589763431911193692017-03-23T18:56:00.000-04:002017-03-23T18:56:12.037-04:00Gluconeogenesis Precursors<div dir="ltr" style="text-align: left;" trbidi="on">
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This video is for quick review for USMLE step1 on precursors of gluconeogenesis and important enzymes. Some of the precursors discussed are alanine, lactate, glycerol and propionyl CoA. All important enzymes of gluconeogenesis is covered in the quick review on gluconeogenesis for USMLE step1.<br />
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Video link for detailed gluconeogenesis process<br />
https://www.youtube.com/watch?v=vBCUbVdad8c&t=238s</div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-41359781201579352182017-03-23T18:53:00.000-04:002017-03-23T18:53:12.609-04:00Glycogen Storage Diseases<div dir="ltr" style="text-align: left;" trbidi="on">
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This video is a super fast high yield review for those who need a quick recap of all glycogen storage disorders for their step1 USMLE review or for any exam review. In this video I have covered all glycogen storage disorders like Von Gierke disease, Pompe disease, McArdle disease, Tarui disease, Hers disease, Andersen disease, Cori's disease. All high yield points are covered about all glycogen storage disorders.<br />
Links for my videos on individual glycogen storage disorders are as below.<br />
Von Gierke disease<br />
https://www.youtube.com/watch?v=v9rmg_pdSt8<br />
Pompe disease<br />
https://www.youtube.com/watch?v=52g5YrExNWY&t=7s<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-67360078101205963812017-03-23T18:49:00.001-04:002017-03-23T18:49:57.240-04:00I Cell Disease<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained about chemical markers for protein targeting. Special focus is on mannose 6 phosphate marker for lysosomes. Lysosomal enzyme targeting to lysosomes with mannose 6 phosphate receptor. i cell disease is inclusion cell disease due to defect in GlcNAc phosphotransferase. The signs and symptoms are similar to hurler syndrome.<br />
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Link for Hurler syndrome<br />
https://www.youtube.com/watch?v=1BcZkRxxc4Y<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-20123738642856016232017-03-19T13:51:00.000-04:002017-03-19T13:51:01.507-04:00Paraxysmal Nocturnal Hemoglobinuria (PNH)<div dir="ltr" style="text-align: left;" trbidi="on">
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This video is all about a rare clonal hematopoetic disorder called paroxysmal nocturnal hemoglobinuria abbreviated as PNH. PNH is because of the mutation in PIG A gene which codes for GPI (glycophosphotidylinositol). GPI is needed for anchoring DAF and CD59 on red cell membrane. In the absence of DAF and CD59 the red cells will be hemolysed by the compliment system. Complimented mediated hemolysis in paroxysmal nocturnal hemoglobinuria, PNH, leads to complement mediated intravascular hemolysis giving rise to hemoglobinuria, jaundice and anemia. PNH is diagnosed using sucrose hemolysis test or sugar water test, Hams test and flow cytometry. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-31147253275327448262017-03-19T13:48:00.000-04:002017-03-19T13:48:24.190-04:00Proteoglycans and Glycosaminoglycans<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained all that you need to know in proteoglycans and glycosaminoglycans. All in brief and high yield points.</div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-70248232593999943102017-03-19T13:45:00.000-04:002017-03-19T13:45:01.512-04:00Hurler Syndrome, Hunter Syndrome and Sanfilippo Syndrome<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained all the high yield and most important things that you need to remember for Hurler syndrome, hunter syndrome and Sanfilippo syndrome. All the things you will need while you prepare for USMLE step1 for these three disorders.<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-52121781432833591722017-03-19T13:41:00.000-04:002017-03-19T13:41:16.082-04:00Integration of Glucose and Galactose Metabolism<div dir="ltr" style="text-align: left;" trbidi="on">
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This video is about how glucose metabolism is linked to galactose metabolism. Glucose oxidation product glucose 1-phosphate is converted to UDP-glucose which is need ed for galactose metabolism. I have explained important enzymes involved in the conversion pathway. I have highlighted the applied aspects in the video. Importance of UDP-glucose in variety of reactions has been explained.<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-33067938983827146892017-03-18T15:15:00.000-04:002017-03-18T15:15:44.352-04:00Brown Adipose Tissue <div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained briefly about three types of adipose tissues: white adipose tissue, brown adipose tissue and biege adipose tissue. The brown adipose tissue is abundantly seen in neonates and the quantity of it decreases as neonate develops into infant, child, adolescent and adult.<br />
Brown adipose tissue has more mitochondria with high expression of an uncoupler protein called thermogenin. Thermogenin is also referred as uncouplin protein 1 (UCP1). Thermogenin acts as uncoupler of electron transport chain and uncouple oxidation from phosphorylation in electron transport chain. This way thermogenin in brown adipose tissue decreases the efficiency of electron transport chain thereby decreasing effective ATP generation from substrate oxidation.<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-17352654976581072902017-03-18T15:12:00.000-04:002017-03-18T15:12:48.988-04:00ATPs from Glucose Oxidation<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained net ATPs coming from oxidation of glucose. While explaining the glycolysis process, I have explained net ATPs coming from oxidation of glucose to 2 pyruvate under aerobic condition. ATPs coming from glycolysis under anaerobic condition, anaerobic glycolysis and ATPs coming from complete oxidation of glucose into 6 CO2 in the TCA cycle. I have also covered difference in the ATP yield both using malate aspartate shuttle and glycerol phosphate shuttle. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-2537489304400558662017-03-18T15:09:00.000-04:002017-03-18T15:09:28.794-04:00Pathophysiology of Diabetes Ketoacidosis (DKA)<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have the pathophysiology of diabetes ketoacidosis seen primarily in type 1 diabetes mellitus. Absolute deficiency of insulin leads to increase in glucagon and decreased peripheral utilization of glucose leading to increased blood glucose level. Increased glucagon along with catecholamines and cortisol leads to increased gluconeogenesis thereby outpouring of glucose from liver into blood which increases blood glucose level. Increased lipolysis leads to increased free fatty acids leading to increased generation of ketone bodies. Increased ketone bodies like acetoacetate and beta-hydroxybutyrate in the blood lead to decrease in blood pH leading to metabolic acidosis. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-41432857092736126892017-03-18T15:06:00.000-04:002017-03-18T15:06:15.367-04:00Why Breakfast is Called as Breakfast?<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained why breakfast is called as breakfast. Before I explained the reason why breakfast is called as breakfast I have explained some of the definitions like absorptive state (post postprandial state), post absorptive state and fasting state. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-75133268999001935252017-03-18T15:03:00.000-04:002017-03-18T15:03:32.686-04:00Gout - Causes and Manifestation<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained about gout, biochemical causes for hyperuricemia like HGPRTase deficiency, glucose 6 phosphatase deficiency, secondary to cancer chemotherapy and radiotherapy or chemoradiation, psoriasis, cancer or change in kinetics of PRPP synthetase. In this video also I have touched upon the composition of gout and pseudogout, differences between gout and pseudogout .<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-11162423189569365702017-03-18T15:00:00.000-04:002017-03-18T15:00:29.042-04:00Jaundice - Types and Causes of Jaundice<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained about different types of jaundice, that is pre-hepatic jaundice, hepatic jaundice and post hepatic jaundice. Various points to differentiate between these three types of jaundice were explained. The enzyme changes, type of bilirubin elevated and the changes in the color of stool and urine is also explained. With the help of this video you should be able to differentiate at-least biochemically three different types of jaundice.<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-19026602875972904312017-03-18T14:56:00.000-04:002017-03-18T14:56:18.747-04:00Protein Digestion and Gastrointestinal Proteases<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained about the digestive proteases both in the stomach and in the intestine. While explaining the dietary protein digestion I have concentrated on the digestive proteases both in the stomach and in the intestine. I have also explained the activation process of zymogen into active enzymes. The specificities of these active proteases like pepsin, trypsin, chymotrypsin, elastase, carboxypeptidase A, carboxypeptidase B, amino peptidase and intracellular peptidase is explained.<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-23384598500939527432016-11-13T16:40:00.000-04:002016-11-13T16:40:07.367-04:00Regulation of Fatty Acid Oxidation<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained the regulation of fatty acid oxidation in the mitochondria. The regulation is mainly going on over outer mitochondrial membrane. The main regulatory molecule is malonyl CoA controlling the activity of CPT I or CAT I.</div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-55020515174209664132016-11-13T16:35:00.000-04:002016-11-13T16:35:35.068-04:00Carnitine Shuttle Mechanism <div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained the carnitine shuttle mechanism for transport of long chain fatty acids into the mitochondrial matrix for beta oxidation. Carnitine is synthesized in the liver using essential amino acids lysine and methionine. Carnitine shuttles back and forth between matrix and inter membrane space to transport LCFA into the matrix.<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-83531727479539414702016-11-13T16:33:00.005-04:002016-11-13T16:37:20.579-04:00Beta Oxidation of a Fatty Acid<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained all the reactions involved in beta-oxidation of even number saturated fatty acid. Beta oxidation of a fatty acid will take place in the mitochondrial matrix. Fatty acid will be oxidized into acetyl CoA which will undergo TCA cycle and ketone body synthesis. Oxidation of fatty acid needs sufficient riboflavin and niacin to maintain the coenzyme needs. Defect in oxidation can lead to impaired ATP generation under fasting condition. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-19966419358695280572016-11-13T16:31:00.001-04:002016-11-13T16:31:47.388-04:00Introduction to Lipoproteins<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained the basic points about lipoproteins. In introduction to lipoproteins I have explained the general structure of lipoproteins, the arrangement of most of the components of lipoproteins including apolipoproteins. Also I have explained the arrangement of lipoproteins according to the density, size, electrophoretic mobility, all the major apolipoproteins and other important apolipoproteins over lipoproteins.<br />
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Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-13893146443248905872016-11-13T16:29:00.001-04:002016-11-13T16:29:40.001-04:00Surfactant and Infant Respiratory Distress Syndrome (IRDS)<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained about surfactant, composition of surfactant, differentiation of pneumocytes into type I pneumocytes and type II pneumocytes. Type of phospholipid in surfactant the major being dipalmitoyl phosphotidyl choline which is also called as dipalmitoyl lecithin. Deficiency of surfactant is seen in pre-mature babies and it will lead to infant respiratory distress syndrome which is seen shortly after birth with apnea, tachycardia, respiratory grunting, flaring of nostril, cyanosis, chest wall retraction, atelectasis, ground glass appearance with air branchogram. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-20510098278800796562016-10-19T12:47:00.000-04:002016-10-19T12:47:33.910-04:00Essential Fructosuria and Hereditary Fructose Intolerance <div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained about two disorders related with fructose metabolism that is essential fructosuria and hereditary fructose intolerance. Essential fructosuria is due to fructokinase deficiency and hereditary fructose intolerance is due to aldolase B deficiency. Patients with hereditary fructose intolerance will have nausea, vomiting, diarrhea, intolerance to fructose, jaundice, liver damage, kidney damage, convulsion, seizures, coma. Essential fructosuria is asymptomatic condition with only elevated levels of fructose in blood and urine. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-83761897595739251982016-10-12T20:26:00.000-04:002016-10-12T20:26:45.170-04:00One Carbon Metabolism<div dir="ltr" style="text-align: left;" trbidi="on">
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In this video I have explained about one carbon metabolism reactions and the donors and formation of one carbon derivatives. Tetrahydrofolate (THF) plays a central role in one carbon metabolism. Vitamin B12, B6 and B2 that is cobalamin, pyridoxine and riboflavin, respectively, helps in the formation of one carbon derivatives from THF. One carbon metabolism participates in synthesis of thymidylate monophosphate, C2 and C8 of purine ring, synthesis of glycine from serine and conversion of homocystienine into methionine. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0tag:blogger.com,1999:blog-838379440750227671.post-84385142567339515032016-10-12T20:24:00.000-04:002016-10-12T20:24:42.701-04:00Why Electrons flow from NADH to O2 in Electron Transport Chain<div dir="ltr" style="text-align: left;" trbidi="on">
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<iframe width="320" height="266" class="YOUTUBE-iframe-video" data-thumbnail-src="https://i.ytimg.com/vi/bZ4XXjQRlV4/0.jpg" src="https://www.youtube.com/embed/bZ4XXjQRlV4?feature=player_embedded" frameborder="0" allowfullscreen></iframe></div>
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In this video I have explained the fundamental basis of electron transport chain that is the redox potential of NADH which is a electron donor and O2 which is a final electron acceptor. Electron transport chain which also referred as oxidative phosphorylation or respiratory chain runs with the redox potential difference of 1140 mv between NADH and O2. This drives flow of electrons from NADH to O2 via complex I, CoQ, III, cytochrome C and complex IV. The energy in the flow of electrons helps in pumping of protons across the membrane. </div>
Dr.Prakash Mungli, MDhttp://www.blogger.com/profile/10953945716132658595noreply@blogger.com0