Correlation
Q: Define Nucleotides. (Topic: Nucleotides)
A: Nucleotides are basic units of nucleic acids made up of nitrogenous base (purine/pyrimidine), pentose sugar & phosphate.
Q: Name the nucleotide which is the universal energy currency of living systems. (Topic: Nucleotides)
A: ATP
Q: Name the nucleotide which acts as second messenger in hormonal action. (Topic: Nucleotides)
A: Cyclic nucleotides such as cAMP and cGMP act as ‘second messengers’
Q: Name the nicotinamide and flavin nucleotides. (Topic: Vitamins)
A: NAD+, NADP+ are 2 coenzymes from niacin (Vitamin B3)
FMN, FAD are 2 coenzymes from riboflavin (Vitamin B2).
Q: Pentose sugar, which is present in Nucleotides, is synthesized in which pathway in carbohydrates metabolism. (Topic: Carbohydrates)
A: HMP shunt
Q: Name the synthetic nucleotide which is used in treatment of Gout. (Topic: Enzymes)
A: Allopurinol is used in the treatment of hyperuricemia and gout. It competitively inhibits enzyme xanthine oxidase.
Q: Name the synthetic nucleotides which is used in treatment of cancer. (Topic: Oncogenesis)
A: Synthetic nucleosides, cytarabine and vidarabine in which ribose is replaced by arabinose are used in chemotherapy to treat cancers.
Synthetic analogues such as 6-mercaptopurine, 5-fluorouracil, 5-iodouracil, 3-deoxyuridine, 5 or 6-azauridine, 5- or 6-azacytidine, 8-azaguanine, 6-thioguanine are widely used by oncologists. They are incorporated into DNA just before cell division, thus blocking cell proliferation.
Q: Name the synthetic nucleotides which is used in treatment of AIDS. (Topic: Nucleotides)
A: Drugs like zidovudine which are used in the treatment of AIDS are synthetic nucleotide analogues with alterations in the sugar structure.
Correlation
Q: Define tophi. (Topic: Nucleotides)
A: Monosodium urate crystals are deposited in the synovium and synovial fluid of the joints causing excruciating joint pain associated with swelling and redness. This inflammatory condition is known as ‘gout’ (gouty arthritis). Monosodium urate crystal deposits slowly increase; they accumulate in the soft tissues and is known as tophi.
Q: Which is the classical site affected in gout? (Topic: Nucleotides)
A: Monosodium urate salt is minimally soluble and hence can be easily precipitated at lower temperatures. Since the intra-articular temperatures of the peripheral joints (small joints of hands and feet) are relatively lower, they are the most commonly affected. The first MTP joint (the great toe) is the classical site affected by gouty arthritis.
Q: Mention the causes of primary gout. (Topic: Nucleotides)
A: Under excretion of uric acid
- Diet rich in purines/alcohol; deficient in dairy products
- Increased purine degradation
- Increased PRPP Synthetase activity
- Decreased/partial HGPRT activity
- HGPRT deficiency
- Glucose-6-phosphatase deficiency
- Abnormal variant of glutathione reductase
Q: Glucose-6-phosphatase enzyme belongs to which pathway? (Topic: Carbohydrates)
A: Gluconeogenesis;
Q: Deficiency of enzyme glucose-6-phosphatase leads to? (Topic: Carbohydrates)
A: Von Gierke’s disease (Type I Glycogen storage disease)
Q: Laboratory diagnosis of which vitamin is done by measurement of FAD-dependent glutathione reductase activity in RBC? (Topic: Vitamins)
A: Vitamin B2- Riboflavin
Q: Name the trace element which is an integral component of enzyme glutathione reductase. (Topic: Minerals)
A: Selenium
Q: Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) enzyme belongs to which pathway? (Topic: Nucleotides)
A: Purine salvage pathway
Q: Inherited deficiency of HGPRT enzyme leads to? Mention its features. (Topic: Nucleotides)
A: Lesch–Nyhan syndrome: Genetic disorder is characterised by spasticity, mental retardation, self-injurious behaviour and gout
Correlation
Q: What is starvation? (Topic: Integration)
A: When the fasting state is prolonged, it results in starvation. May be due to food scarcity or the desire to rapidly lose weight or certain clinical conditions (surgery, burns etc.)
Q: Mention the effect of starvation on gluconeogenesis. (Topic: Carbohydrates)
A: During starvation – Excess lipolysis – Acetyl CoA accumulates – Promotes gluconeogenesis.
Q: Mention the major pathways which are involved in energy production during starvation. (Topic: Integration)
A: Glycogenolysis, Gluconeogenesis, Fatty Acids oxidation, Ketogenesis
Q: Define and mention the rate limiting enzyme of glycogenolysis. (Topic: Carbohydrates)
A: Glycogenolysis: Breakdown of glycogen to glucose.
Glycogenolysis- Rate limiting enzyme is Glycogen phosphorylase
Q: Define and mention the rate limiting enzyme of gluconeogenesis. (Topic: Carbohydrates)
A: The synthesis of new glucose or glycogen from non-carbohydrate sources is called gluconeogenesis. Key enzymes in Gluconeogenesis:
- Pyruvate carboxylase
- Phosphoenol pyruvate carboxykinase
- Fructose 1,6 Bis-phosphatase
- Glucose 6-phosphatase
Q: During starvation, which organ becomes an important site of gluconeogenesis and may contribute as much as half of the blood glucose. (Topic: Integration)
A: Kidney
Q: Define and mention the rate limiting enzyme of fatty acid oxidation. (Topic: Lipids)
A: Oxidation of fatty acids on β-carbon atom; Acyl CoA dehydrogenase
Q: Define and mention the rate limiting enzyme and precursor of ketogenesis. (Topic: Lipids)
A: Synthesis of ketone bodies; Exclusively in Liver- Mitochondrial matrix.
Acetyl CoA (from Beta Oxidation of Fatty Acids) as precursor.
HMG CoA synthase is the rate limiting step.
Q: During starvation which organ adapts to utilize ketone bodies. (Topic: Integration)
A: Brain
Correlation
Q: Mention the changes in hormones of blood sugar regulation in starvation (Topic: Integration)
A: Decrease in Insulin/ Glucagon ratio.
Q: Mention the changes in RQ (Respiratory Quotient) in starvation. (Topic: Nutrition)
A: RQ Decreases; Initial 1 to 2 days: 0.78 (stored glycogen); Later: 0.7(fat combustion)
Q: Define Respiratory Quotient (RQ). (Topic: Nutrition)
A: Definition: Ratio of volume of CO2 produced by the volume of O2 consumed (CO2/ O2) in the oxidation of foodstuffs during a given time
Q: Mention the changes in BMR in starvation. (Topic: Nutrition)
A: During starvation, energy intake has an inverse relation with BMR; Decreases upto 50%
Q: Starvation leads to which type of acidosis? (Topic: Acid-Base Balance)
A: Starvation ketoacidosis- Metabolic acidosis
Q: Which amino acid is transported mostly in starvation from muscle to liver. (Topic: Carbohydrates)
A: Glucose Alanine Cycle: Transport of Amino acid (alanine dominates) from muscle to liver, mainly in starvation. Alanine is transported to liver and utilized for gluconeogenesis.
Q: Why starvation and uncontrolled diabetes mellitus leads to ketosis?
A: Prolonged Starvation & uncontrolled DM- main causes of ketosis. (Topic: Integration)
Carbohydrate is either unavailable (starvation) or underutilized (diabetes)- Oxaloacetate is unavailable for combining with acetyl CoA Impaired TCA cycle- Acetyl CoA is diverted for KB synthesis.
Q: Mention the test to detect ketone bodies in urine. (Topic: Integration)
- A: Rothera’s Nitroprusside test:
Answered by Acetoacetate and acetone.
- Gerhardt’s Ferric Chloride Test:
Answered by Acetoacetate
- KB that cannot be detected by both Tests:
β- hydroxybutyrate
Q: Mention the mechanism of fatty liver in starvation. (Topic: Integration)
A: In Diabetes mellitus, starvation, high fat diet: Increased mobilization of FFA from adipose tissue and their influx into liver is much higher than utilization.
Correlation
Q: Describe structure of hemoglobin. (Topic: Hemoglobin)
A: Conjugated globular Tetrameric allosteric protein
Non protein component: Heme; Protein component: Globin
Four subunits of Hb are held together by non-covalent interactions: hydrophobic, ionic, hydrogen bonds.
Q: Name the mineral which is present in hemoglobin. (Topic: Minerals)
A: About 75% of iron occurs in the RBC as a constituent of hemoglobin.
Q: Other than heme, name other iron containing substances. (Topic: Minerals)
A: Hemoglobin, Myoglobin, cytochrome, xanthine oxidase, catalase, tryptophan pyrrolase, peroxidase
Q: Name antioxidant enzymes. (Topic: Antioxidant Defense System)
A: Catalase, Superoxide dismutase (SOD), Glutathione peroxidase and reductase
Q: Mention the composition of adult hemoglobin HbA1 and glycosylated hemoglobin HbA1C. (Topic: Hemoglobin)
A: HbA1: Alpha 2- Beta 2
HbA1C: Alpha 2- Beta 2- Glucose
Q: Mention clinical significance of HbA1C. (Topic: Carbohydrates)
A: Directly related to exposure of RBC to glucose: Indicates blood glucose concentration over 2-3 months (half life of RBC).
Q: Mention the diagnostic criteria of HbA1C for diabetes mellitus. (Topic: Carbohydrates)
A: Normal: < 5.7 gm%
Impaired glucose tolerance: 5.7-6.4 gm%
Diabetes Mellitus: > 6.5 gm%
Correlation
Q: Name the hemoglobin derivatives. (Topic: Hemoglobin)
A: Hemoglobin (specifically heme) combines with different ligands and forms hemoglobin derivatives. OxyHb, DeoxyHb, Methemoglohin (metHb), Carboxyhemoglobin (COHb)
Q: Mention Hemoglobin abnormalities. (Topic: Hemoglobin)
A: Quantitative abnormalities: Decrease production of normal hemoglobins
Ex. alpha Thalassemia, beta Thalassemia
Qualitative abnormalities: Production of abnormal hemoglobin Ex. sickle cell anemia.
Q: Mention the molecular defect in sickle cell. (Topic: Nucleic acids)
A: (HbS): two normal α-globin chains and two abnormal (point missense mutation) β-globin chains. This is due to a difference in a single amino acid. In HbS, glutamate (Polar) at sixth position of β-chain is replaced by valine (non-polar).
Q: Difference between sickle cell trait and disease. (Topic: Hemoglobin)
A: Homozygous- caused by inheritance of two mutant genes (one from each parent) that code for β-chains.
Heterozygous- only one gene (of β-chain) is affected while the other is normal.
The erythrocytes of heterozygous contain both HbS and HbA and the disease is referred to as sickle cell trait. The individuals of sickle-cell trait lead a normal life, and do not usually show clinical symptoms.
Q: Mention the use of polymerase chain reaction (PCR) in diagnosis of Sickle cell disease and thalassemia. (Topic: Recombinant DNA Technology)
A: PCR is widely used in the diagnosis of genetic disorders. The gene segments that contain mutations are amplified to enable diagnosis of inherited diseases such as sickle cell anemia, cystic fibrosis, beta-Thalassemia etc.
Q: Mention the diagnostic role of electrophoresis in Sickle cell. (Topic: Hemoglobin)
A: When subjected to electrophoresis in alkaline medium (pH 8.6) , sickle-cell hemoglobin (HbS) moves slowly towards anode (positive electrode) than does adult hemoglobin (HbA).
The slow mobility of HbS is due to less negative charge, caused by the absence of glutamate residues that carry negative charge.
Q: Name the type of jaundice, which sickle cell disease will cause? (Topic: Hemoglobin)
A: Hemolytic jaundice
Correlation:
Q: Mention types of alpha thalassemia. (Topic: Hemoglobin)
A: Silent carrier (1 missing gene), alpha thalassemia trait (2 missing genes), Hb H disease (3 missing genes), Hydrops fetalis (4 missing genes).
Q: Mention types of beta thalassemia. (Topic: Hemoglobin)
A: β-thalassemia major: Homozygous state with a defect in both the genes responsible for β-globin synthesis.
β-thalassemia minor: Heterozygous state with a defect in only one of the two β-globin gene pairs on chromosome 11. Also known as β -thalassemia trait
Q: Mention the defect in beta-thalassemia with transcription. (Topic: Nucleic acids)
A: β-Thalassemia: Faulty splicing
Due to mutation resulting in nucleotide change at exon-intron junction
Diminished or lack of synthesis of β–chain of Hb.
Q: Patient with β-thalassemia major requires which type of treatment? (Topic: Nucleic acids)
A: Healthy at birth since β – globin is not synthesized during the fetal development.
They become severely anemic and die within 1-2 years.
Frequent blood transfusion is required for these children.
Q: Mention the condition in patients receiving frequent blood transfusions. (Topic: Minerals)
A: Hemosiderosis
Q: Name the other condition in which Iron directly deposited in the tissues (Liver, spleen, pancreas, skin), also known as bronze diabetes. (Topic: Minerals)
A: Hemochromatosis
Q: Mention the condition of iron deficiency. (Topic: Minerals)
A: Iron deficiency anaemia: Most prevalent nutritional disorder worldwide
Microcytic hypochromic anaemia
Correlation:
Q: Name the rate limiting enzyme of heme synthesis. (Topic: Hemoglobin)
A: ALA synthase (amino levulinic acid synthase)
Q: Which amino acid is required for heme synthesis. (Topic: Amino Acids & Proteins)
A: Glycine
Q: Name the Kreb’s cycle intermediate required for heme synthesis. (Topic: Carbohydrates)
A: Succinyl CoA
Q: Name the coenzyme required for ALA synthase enzyme. (Topic: Vitamins)
A: Pyridoxal phosphate (vitamin B6) is a coenzyme for this reaction.
Q: Name the diseases associated with heme synthesis. (Topic: Hemoglobin)
A: Porphyria
Q: Name the cofactor needed for enzyme ALA synthase. (Topic: Minerals)
A: Copper is a cofactor of ALA synthase (heme synthesis), it is required for the formation of hemoglobin, myoglobin and cytochromes.
Q: Mention the regulation of heme synthesis. (Topic: Hemoglobin)
A: Feedback inhibition by heme. Repression of enzyme ALA synthase.
Q: Describe Gene regulation by Repression. (Topic: Nucleic acids)
A: Regulatory gene produce Apo-repressor;
Structural gene (enzyme ALA synthase) produces heme (Co-repressor)
Holo-repressor (Apo+ Co): binds operator: stops transcription.
When heme (Co-repressor) not available- Repression not effective- Enzyme ALA synthase synthesis (heme) starts.
Correlation:
Q: Mention the biochemical picture of obstructive jaundice. (Topic: Hemoglobin)
A: Increased conjugated Bilirubin, Significant Rise in Enzyme ALP, Dark colored urine, Clay colored stool due to absence of stercobilinogen.
Q: Mention the effect of obstructive jaundice on serum cholesterol levels? (Topic: Lipids)
A: Hypercholesterolemia
Q: Mention the vitamin deficiency which occurs in patients of obstructive jaundice? (Topic: Vitamins)
A: Vitamin K deficiency is seen in adults suffering from obstructive jaundice and other diseases causing severe fat malabsorption.
Q: Mention the causes of obstructive jaundice. (Topic: Hemoglobin)
A: Caused by gallstones, Ca head of pancreas, Ca of common bile duct etc
Q: Mention the result of Van den Bergh test in obstructive jaundice. (Topic: Organ function Tests)
A: Van den Bergh- Direct Positive
Q: Mention the test for bilirubin in urine. (Topic: Organ function Tests)
A: Van den Bergh’s test, Gmelin’s test, Cole’s test, Fouchet’s test, Ehrlich’s test
The presence of bilirubin in urine suggests the increased level of conjugated bilirubin in blood which is due to hepatic or obstructive jaundice.
Q: Mention the test for bile salts in urine. (Topic: Organ function Tests)
Bile salts are excreted along with bile pigments and these are detected by
Hay’s sulphur powder test, Pettenkoffer’s test, Oliver’s test
Bile salts are excreted in urine in Obstructive Jaundice and may be in hepatocellular Jaundice.
Q: Mention other enzyme than ALP which is elevated in obstructive jaundice. (Topic: Organ function Tests)
A: Elevated level of 5’-Nucleotidase is seen in obstructive liver disease (hepatobiliary disease). It’s activity is parallel to that of ALP.
Correlation:
Q: Mention the biochemical picture of hepatic jaundice. (Topic: Hemoglobin)
A: Increased both conjugated and unconjugated Bilirubin, Significant Rise in liver Enzymes ALT & AST, Van den Bergh test- Biphasic
Q: Mention the causes of hepatic jaundice. (Topic: Hemoglobin)
A: Causes – Viral hepatitis, cirrhosis of liver, cardiac failure, poisons and toxins, Drugs etc.
Q: ALT or AST, which is more sensitive for liver diseases. (Topic: Enzymes)
A: The levels of ALT & AST in serum are elevated in all liver diseases but ALT is more sensitive & reliable.
Q: Name the isoenzyme which is elevated in liver diseases. (Topic: Enzymes)
A: LDH 4 & LDH5
Q: How much bilirubin is daily produced in adults? (Topic: Hemoglobin)
A: About 6 g of Hb is broken down & resynthesized per day in an adult man. One gram of Hb on destruction finally yields 35 mg of bilirubin. Approximately 250-350 mg of bilirubin is daily produced in adults.
Q: Mention the detoxification of bilirubin by liver. (Topic: Xenobiotics)
A: Unconjugated (Insoluble) bilirubin is converted to conjugated (soluble) bilirubin by hepatic enzyme UDP- Glucuronyl transferase.
Q: Bilirubin is transported with? (Topic: Amino Acids & Proteins)
A: Albumin has two binding sites for bilirubin- a high affinity site & a low affinity site. Approximately 25 mg bilirubin can bind can tightly bind to albumin (at high affinity sites) per 100 ml of plasma.
Correlation:
Q: Mention the biochemical picture of hemolytic jaundice. (Topic: Hemoglobin)
A: Increased Unconjugated Bilirubin, Van den Bergh- Indirect Positive, No rise in liver Enzymes. Urobilinogen positive in urine
Q: Hay’s sulfur powder test and Fouchet’s test will be Negative in which type of jaundice? (Topic: Organ function Tests)
A: Hemolytic jaundice
Q: Mention the effect of hemolytic jaundice on serum cholesterol levels? (Topic: Lipids)
A: Hypocholesterolemia
Q: Mention the causes of hemolytic jaundice. (Topic: Organ function Tests)
A: Excess Hemolysis may be due to Incompatible Blood Transfusion, Malaria, Sickle Cell Disease, Deficiency of G-6PD enzyme etc
Q: Which condition can result in a hyperbilirubinemic toxic encephalopathy, or kernicterus, causing mental retardation? (Topic: Hemoglobin)
A: Neonatal physiological jaundice
Q: Mention the mechanism of neonatal physiological jaundice. (Topic: Hemoglobin)
A: Not only is the bilirubin-UGT activity reduced, but there probably is reduced synthesis of the substrate for that enzyme, UDP-glucuronic acid.
Since the increased amount of bilirubin is unconjugated, it is capable of penetrating the blood-brain barrier when its concentration in plasma exceeds that which can be tightly bound by albumin (20–25 mg/dL).
Q: Mention the inherited conditions of indirect hyperbilirubinemia and direct bilirubinemia. (Topic: Hemoglobin)
A: Indirect hyperbilirubinemia
- 1. Crigler-Najjar types I and II
- 2. Gilbert’s syndrome
Direct hyperbilirubinemia
- 1. Dubin-Johnson syndrome
- 2. Rotor’s syndrome