Channel Title: Biochem Simplified Channel Description: <video> Maintenance of Blood pH II Buffers II Acid-base Balance Part 1 Description: To maintain blood pH at 7.35- 7.45 Three primary system Buffer system – First line of defence Respiratory mechanism –Second line defence Renal mechanism – Third line defence Death will occur if blood pH goes below 7.0 or above 7.8. Equation valid for any buffer pair The general equation referred to as Henderson Hasselbalch equation for any buffer is written as PH = PKa + log [Base] [Acid] Evident- PH dependant on the ratio of conc of base & acid Buffering capacity depends on the concentration of the buffer and pKa. pKa is the pH at which buffer exists in equal proportion with its acid and conjugate base A buffer is considered effective with ± 2 pH of its pKa It has maximum buffering capacity when pKa = pH For maximum buffering capacity, the pKa should be near the physiological pH 7.4 Bicarbonate buffer Bicarbonate is the most important buffer system in the body due to Its high concentration and the two elements of the bicarbonate system HCO3 & H2CO3 can be easily regulated Phosphate Buffer Not Important blood buffer but play a major role in buffering renal tubular fluid & intracellular fluids Protein Buffers Plasma protein & Hemoglobin (Hb) constitute protein buffer system Hemoglobin Buffers Major intracellular buffer present in erythrocytes Since hemoglobin is present in very high concentration and Is rich in histidine (38) residues, its buffering capacity is much higher than plasma proteins Makes Hb dominant buffering agent of blood at physiological pH It buffers carbonic acid & its anhydride CO2 from tissues </video> <video> Respiratory and Renal mechanism in Acid-base balance II Regulation of Blood pH II Part 2 Description: Respiratory mechanism of Acid-base balance The second line of defense against acid-base disturbances is by regulating the concentration of carbonic acid (H2CO3) in the blood and other body fluids by the lungs Rapid mechanism The respiratory center regulates the removal or retention of CO2 & thereby H2CO3 from ECF by the lungs. But temporary basis – till renal mechanism – the permanent restoration of pH. The rate of ventilation increases- when an increase in acid –then excess H2CO3 in the form of CO2 quickly removed Similarly when the rate of ventilation decrease, acid (H2CO3) in form of CO2 is added to neutralize excess alkali (HCO3) The renal mechanism is the third line of defense in acid-base balance Long term acid-base control is exerted by renal mechanisms Tries to provide a permanent solution, contrast to temporary buffer & short-term respiratory mechanism. Kidney participates by conservation HCO3– alkali reserve & excretion acid Renal conservation of HCO3 & excretion of acid occurs through four key mechanism: 1.Exchange of H + for Na + of tubular fluids 2. Reabsorption (reclamation) bicarbonate from tubular fluid 3. Formation ammonia & excretion ammonium ion (NH4+) in urine 4. Excretion H+ as H2PO4- in urine </video> <video> Ketone bodies: Ketogenesis & Utilization II Ketosis- Ketonemia II Ketouria II Diabetic Ketoacidosis Description: Acetone, acetoacetic acid, and β-hydroxybutyric acid are called ketone bodies Normally these are produced from fatty acids in a very small amount so that blood level is less than 1 mg/dl and urinary excretion is negligible </video> <video> Lipoproteins II Structure II Classification II Composition II Function Description: Lipids absorbed from the diet and synthesized by the liver and adipose tissue must be transported between various cells and organs for utilization and storage Lipids are insoluble in water -the problem of transportation in the aqueous plasma Associate nonpolar lipids (triacylglycerols and cholesteryl esters) with amphipathic lipids (phospholipids and cholesterol) and proteins to make water-miscible lipoproteins. Classes of Lipoproteins 1. Chylomicrons are synthesized from dietary fats in the small intestine. They transport the exogenous lipids for utilization to peripheral tissues 2. VLDL (Very low density lipoprotein or pre β lipoprotein) Synthesized in the liver and transport endogenous lipids like TAG, cholesterol etc. for utilization to peripheral tissues 3. LDL (Low density lipoprotein) is rich in cholesterol and transport it to peripheral tissues 4. HDL (High density lipoprotein) Synthesized both liver and intestines. Reserve cholesterol transport Free fatty acid (FFA) although not a lipoproteins but is an important lipid fraction in serum </video> <video> Beta Oxidation of Fatty acids Part I Description: </video> <video> Therapeutic enzymes II Justifications II Short questions II Description: Enzymes used for the treatment of a particular disease are known as Therapeutic enzymes. Enzymes often bind & act on their targets with great affinity & specificity. Enzymes are catalytic & convert multiple target molecules to the desired products. These two features make enzymes specific & potent drugs. They have a broad variety of specific uses as Oncolytics Anticoagulants Thrombolytics Replacements for metabolic deficiencies Digestive aids Metabolic storage disorders, etc </video> <video> Fatty liver II Lipotropic factors Description: Fatty livers fall into two main categories- 1. More synthesis of Triglycerides High carbohydrate diet High fat feeding Alcohol – also inhibits fat oxidation Starvation Diabetes mellitus A high carbohydrate diet stimulates de novo fatty acid synthesis by providing an excess of Acetyl CoA and high fat feeding provides more flux of fatty acids from the diet that can be esterified to provide excess triglycerides. 2. Defective VLDL synthesis -The second type of fatty liver is usually due to a metabolic block in the production of plasma lipoproteins, thus allowing triacylglycerol to accumulate. maybe due to – a. A block in apolipoproteins synthesis b. Protein energy Malnutrition c. Impaired absorption d. Presence of inhibitors of endogenous protein synthesis e.g.- Carbon tetrachloride, Puromycin, Ethionine, Heavy metals, etc.e. Hypobetalipoproteinemia- Defective apo B gene can cause the impaired synthesis of apo B protein. e .Impaired secretion of VLDL- oxidative stress is a common cause for membrane disruption of lipoproteins. Alcoholic fatty liver Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis. Lipotropic agents- Agents such as- Choline betaine Inositol Methionine and other essential amino acids, Essential fatty acids, Anti oxidant vitamins, Vitamin B12, folic acid Glycine , serine and Synthetic antioxidants which have the apparent effect of removal of fats from the liver cells, and thus prevent the formation of fatty liver are called lipotropic agents. </video> <video> HDL metabolism II Good Cholesterol Description: Synthesis of HDL HDL is synthesized and secreted from both the liver and intestine. However, apo C and apo E are synthesized in the liver and transferred from liver HDL to intestinal HDL when the latter enters the plasma. A major function of HDL is to act as a repository for the apo C and apo E required in the metabolism of chylomicrons and VLDL. Nascent HDL consists of a discoid phospholipid bilayer containing apo A and free cholesterol. LCAT and the LCAT activator apo A-I—bind to the discoidal particles, and the surface phospholipid and free cholesterol are converted into cholesteryl esters and lysolecithin. The nonpolar cholesteryl esters move into the hydrophobic interior of the bilayer, whereas lysolecithin is transferred to plasma albumin. Thus, a nonpolar core is generated, forming a spherical, pseudomicellar HDL covered by a surface film of polar lipids and apolipoproteins. This aids the removal of excess unesterified cholesterol from lipoproteins and tissues . Role of LCAT LCAT( Lecithin Cholesterol Acyl Transferase) enzyme catalyzes the esterification of cholesterol to form Cholesteryl ester. The reaction can be represented as follows- Function of CETP: Cholesterol Ester Transport Protein Transfers Cholesterol Molecule from HDL to VLDL & TAG molecule from VLDL to HDL. </video> <video> CK MB is an Isoenzyme/ CK 2 is a cardiac marker. Description: In the new MCI curriculum, almost 50% of questions are asked as objective questions in the form of comments, justification, few line questions, even structured long questions are divided into subsets of two mark questions. This question is asked as a comment as well as a short note. Here I have tried to explain how you can write a comment/justification/ Few sentences questions. </video> <video> Metabolism of chylomicrons Description: </video> <video> Fatty acid synthesis part 1 Description: Fatty acid synthesis part 1 Occur in cytosol Mainly in the liver & lactating mammary gland and to a lesser extent in adipose tissue, kidney & brain. Starting material is Acetyl CoA. Not reversal of oxidation </video> <video> Cholesterol II Synthesis II Regulation II Fate Description: STEPS OF CHOLESTEROL SYNTHESIS 1. Synthesis of HMG CoA 2. Formation of mevalonate 3. Conversion of mevalonate to activated isoprene units 4. Polymerization of six isoprene units to form squalene 5. Cyclization of squalene to form parent steroid nucleus lanosterol and 6. Formation of cholesterol from lanosterol Regulation of cholesterol synthesis: Competitive inhibition Statins (Lovastatin, Mevastatin, Atorvastatin, etc.) are the reversible competitive inhibitors of HMG Co A reductase. They are used to decrease plasma cholesterol levels in patients with hypercholesterolemia. Feedback inhibition HMG Co-A reductase is inhibited by Mevalonate and Cholesterol. Mevalonate is the immediate product of HMG Co-A reductase catalyzed reaction whereas Cholesterol is the ultimate product of the reaction pathway. Covalent modification (Role of hormones) Phosphorylation decreases the activity of the reductase. Glucagon favors the formation of the inactive (phosphorylated form) form, hence decreases the rate of cholesterol synthesis In contrast, insulin favors the formation of the active(dephosphorylated) form of HMG Co A reductase and results in an increase in the rate of cholesterol synthesis Cholesterol synthesis ceases when the ATP level is low Fate : Bile acids & Bile salts Vitamin D3 Steroid hormones </video> <video> Phospholipids Description: Phospholipids are compound lipids, they contain fatty acids, glycerol or other alcohol, a phosphoric acid residue, nitrogen-containing base, and other substituents. Important short notes usually asked for 3 marks. Many MCQs are also asked about this topic. </video> <video> Phenylketonuria (PKU) Case study Description: In my Videos, I am going to show you how you can answer the questions of a case study or the same questions can be asked as justifications . Each question is for 2 marks each, here you will have to give the correct answer in few sentences or you can also use diagrammatic representation as I have shown in my videos. But the diagrams should be self-explanatory, legible, and labeled properly. This is for MBBS students and for PG entrances. </video> <video> Metabolism of VLDL & LDL . LDL is a bad cholesterol Description: When the diet contains more fatty acids & cholesterol they are converted to TAG or cholesterols in the liver & packed with apolipoproteins into the ‘Very low-density lipoproteins (VLDL) Excess carbohydrate in the diet also converted to TAG in the liver and exported as VLDL LDL cholesterol is a bad cholesterol Phagocytic macrophages have nonspecific receptors known as “scavengers” receptors that recognize LDL that has been chemically modified such as oxidized LDL. Foam cells, also called lipid-laden macrophages are a type of cell that contains cholesterol. These can form a plaque that can lead to atherosclerosis and trigger heart attacks and Stroke. LDL rich macrophages (foam cells) migrate into the endothelium and induce inflammation and chemotaxis to initiate the formation of atherosclerotic plaques and possibly thrombosis High levels of LDL cholesterol raise the risk for heart disease and stroke. </video>

Videos from channel