Sample Question on Detoxification (Xenobiotics Metabolism)

Sample Question on Detoxification (Xenobiotics Metabolism)

Sample Question on Lipoprotein Metabolism Up to 4K

Gluconeogenesis Precursors

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.

Video link for detailed gluconeogenesis process
https://www.youtube.com/watch?v=vBCUbVdad8c&t=238s

Glycogen Storage Diseases

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.
Links for my videos on individual glycogen storage disorders are as below.
Von Gierke disease
https://www.youtube.com/watch?v=v9rmg_pdSt8
Pompe disease
https://www.youtube.com/watch?v=52g5YrExNWY&t=7s

I Cell Disease

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.

Link for Hurler syndrome
https://www.youtube.com/watch?v=1BcZkRxxc4Y

Paraxysmal Nocturnal Hemoglobinuria (PNH)

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. 

Proteoglycans and Glycosaminoglycans

In this video I have explained all that you need to know in proteoglycans and glycosaminoglycans. All in brief and high yield points.

Hurler Syndrome, Hunter Syndrome and Sanfilippo Syndrome

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.

Integration of Glucose and Galactose Metabolism

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.

Brown Adipose Tissue

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.
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.

ATPs from Glucose Oxidation

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. 

Pathophysiology of Diabetes Ketoacidosis (DKA)

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. 

Why Breakfast is Called as Breakfast?

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. 

Gout - Causes and Manifestation

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 .

Jaundice - Types and Causes of Jaundice

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.

Protein Digestion and Gastrointestinal Proteases

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.

Regulation of Fatty Acid Oxidation

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.

Carnitine Shuttle Mechanism

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.

Beta Oxidation of a Fatty Acid

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.