Free NEET PG & INI-CET Biochemistry MCQs

Explanation

Km is the substrate concentration at half-maximal velocity. A low Km means the enzyme reaches half of Vmax at low substrate concentration, indicating high affinity for its substrate.

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A competitive inhibitor competes for the active site, raising the apparent Km through reduced affinity, while Vmax is unchanged because high substrate concentrations overcome the inhibition.

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Cardiac troponins T and I are the most specific and sensitive markers of myocardial injury, rising within hours and remaining elevated for days. CK-MB is an older marker.

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Thiamine pyrophosphate, from vitamin B1, is a coenzyme for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase. B1 deficiency impairs these and causes beriberi and Wernicke encephalopathy.

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HMG-CoA reductase catalyses the rate-limiting step of cholesterol synthesis and is the target of statins. HMG-CoA lyase, by contrast, is involved in ketone body formation.

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Transferases move functional groups such as amino or phosphate groups between substrates; the aminotransferases ALT and AST are examples. Oxidoreductases handle redox reactions and hydrolases cleave bonds using water.

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PFK-1 is inhibited by ATP and citrate, both signals of energy abundance, and activated by AMP and fructose-2,6-bisphosphate. This makes it the main control point of glycolysis.

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Glycolysis takes place in the cytoplasm and does not require oxygen. It converts glucose to pyruvate with a net yield of 2 ATP and 2 NADH per glucose molecule.

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The citric acid cycle occurs in the mitochondrial matrix. Each turn generates 3 NADH, 1 FADH2 and 1 GTP, feeding electrons into the electron transport chain for ATP production.

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The liver is the main site of gluconeogenesis, producing glucose from lactate, glycerol and amino acids to maintain blood glucose during fasting. The kidney contributes during prolonged starvation.

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The HMP shunt produces NADPH, for reductive biosynthesis and antioxidant defence, and ribose-5-phosphate for nucleotide synthesis. It does not generate ATP directly.

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In the Cori cycle, muscle lactate travels to the liver, where it is converted back to glucose via gluconeogenesis and returned to muscle. This recycles lactate and supports glucose supply during exercise.

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Molecular oxygen is the final electron acceptor at complex IV, being reduced to water. This maintains electron flow and the proton gradient that drives ATP synthesis; without oxygen the chain halts.

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GLUT4 is the insulin-responsive transporter in skeletal muscle and adipose tissue, and insulin promotes its translocation to the cell membrane. GLUT2 is in liver and pancreatic beta cells, and GLUT5 transports fructose.

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Carnitine shuttles long-chain fatty acids across the inner mitochondrial membrane via the carnitine palmitoyltransferase system. Carnitine deficiency impairs fatty-acid oxidation, causing muscle weakness and hypoglycaemia.

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HDL carries out reverse cholesterol transport, moving cholesterol from peripheral tissues to the liver, and is protective against atherosclerosis. LDL delivers cholesterol to tissues and is atherogenic.

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Apo C-II activates lipoprotein lipase on capillary endothelium, releasing free fatty acids from triglyceride-rich lipoproteins. Apo A-I activates LCAT and Apo B-100 is the ligand for the LDL receptor.

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Ketone bodies, namely acetoacetate, beta-hydroxybutyrate and acetone, are made in liver mitochondria from acetyl-CoA during fasting or diabetic ketoacidosis. Peripheral tissues, including the brain in prolonged fasting, use them for energy.

Explanation

Linoleic acid, an omega-6, and alpha-linolenic acid, an omega-3, are essential because humans cannot synthesise them. They are precursors of arachidonic acid and other signalling molecules.

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Familial hypercholesterolaemia results from defective LDL receptors, impairing LDL clearance and causing very high LDL, tendon xanthomas and premature atherosclerosis. It is inherited in an autosomal dominant pattern.

Explanation

The urea cycle occurs in the liver, partly in mitochondria and partly in cytoplasm, converting toxic ammonia to urea for excretion. Enzyme defects cause hyperammonaemia and encephalopathy.

Explanation

Pyridoxal phosphate, from vitamin B6, is the coenzyme for aminotransferases such as AST and ALT, transferring amino groups between amino acids and keto acids.

Explanation

Lysine is essential and must be obtained from the diet. Others include leucine, isoleucine, valine, threonine, methionine, phenylalanine, tryptophan and histidine. Alanine, glutamate and serine are non-essential.

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Vitamin C, or ascorbate, is a cofactor for prolyl and lysyl hydroxylases, essential for stable collagen triple-helix formation. Deficiency, or scurvy, causes fragile collagen, poor wound healing and bleeding gums.

Explanation

Secondary structure refers to local folding patterns such as the alpha-helix and beta-sheet, stabilised by hydrogen bonds. Primary is the amino-acid sequence, tertiary is the overall three-dimensional fold and quaternary is the assembly of subunits.

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Negative nitrogen balance means nitrogen loss exceeds intake, reflecting net protein catabolism as seen in starvation, trauma, sepsis or severe illness. Positive balance occurs during growth, pregnancy and recovery.

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Thiamine deficiency causes Wernicke encephalopathy, with confusion, ophthalmoplegia and ataxia, and if untreated Korsakoff psychosis. Give thiamine before glucose to avoid precipitating Wernicke encephalopathy.

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Vitamin B12 deficiency causes megaloblastic anaemia with hypersegmented neutrophils plus neurological features, namely subacute combined degeneration. Folate deficiency gives the same haematology but without neurological signs.

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Vitamin C deficiency, or scurvy, impairs collagen synthesis, causing bleeding gums, perifollicular haemorrhages, poor wound healing and corkscrew hairs. Vitamin C is a cofactor for collagen hydroxylation.

Explanation

Vitamin D is hydroxylated first in the liver to 25-hydroxyvitamin D and then in the kidney to 1,25-dihydroxyvitamin D, or calcitriol, the active form. Calcitriol increases intestinal calcium and phosphate absorption.

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Vitamin A, as retinal, is required for rhodopsin in the retina; deficiency causes night blindness, then xerophthalmia and Bitot spots. Vitamin A also maintains epithelial integrity.

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Vitamin K is essential for gamma-carboxylation of clotting factors II, VII, IX and X, as well as proteins C and S. Warfarin inhibits this by blocking vitamin K epoxide reductase.

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Pellagra, with dermatitis, diarrhoea and dementia, results from niacin deficiency. It can also occur in Hartnup disease and carcinoid syndrome, where tryptophan, a niacin precursor, is diverted or lost.

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Southern blotting detects DNA, Northern detects RNA and Western detects protein. Western blot has been used, for example, as a confirmatory HIV test.

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PCR uses heat-stable Taq DNA polymerase to amplify DNA through repeated cycles of denaturation, annealing and extension. Taq's thermostability allows it to survive the high denaturation temperatures.

Explanation

DNA polymerase I uses its 5' to 3' exonuclease activity to remove RNA primers and fills the gaps with DNA. DNA ligase then seals the remaining nicks between Okazaki fragments.

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The code is degenerate, or redundant, because most amino acids are specified by more than one codon. This buffers the effect of some point mutations, especially at the third wobble position.

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Transcription is the synthesis of mRNA from a DNA template by RNA polymerase. Translation then converts the mRNA sequence into protein at the ribosome.

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A nonsense mutation changes a codon to a premature stop codon, truncating the protein. A missense mutation changes one amino acid, a silent mutation causes no amino-acid change and a frameshift shifts the reading frame.

Explanation

Von Gierke disease, glycogen storage disease type I, is due to glucose-6-phosphatase deficiency, blocking the final step of gluconeogenesis and glycogenolysis. This causes fasting hypoglycaemia, hepatomegaly and lactic acidosis.

Explanation

McArdle disease, glycogen storage disease type V, results from muscle glycogen phosphorylase deficiency, causing exercise intolerance, cramps and myoglobinuria, with a characteristic second wind as fatty acids are recruited.

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Phenylketonuria is caused by phenylalanine hydroxylase deficiency, leading to phenylalanine accumulation, a musty odour, fair pigmentation and intellectual disability if untreated. Management is a phenylalanine-restricted diet.

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Alkaptonuria is due to homogentisate oxidase deficiency, causing accumulation of homogentisic acid. Urine darkens on standing, and pigment deposits in connective tissue cause ochronosis and arthritis.

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Classic galactosaemia results from galactose-1-phosphate uridyltransferase deficiency. Galactose-1-phosphate accumulates, causing liver damage, cataracts and, if untreated, sepsis. Treatment is a galactose-free diet.

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Tay-Sachs disease is caused by hexosaminidase A deficiency, leading to GM2 ganglioside accumulation, neurodegeneration and a cherry-red macular spot. Unlike Niemann-Pick disease, there is no hepatosplenomegaly.

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Gaucher disease is the most common lysosomal storage disorder, due to glucocerebrosidase deficiency. Gaucher cells, lipid-laden macrophages with a crumpled tissue paper appearance, accumulate and cause hepatosplenomegaly and bone disease.

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Maple syrup urine disease is due to deficient branched-chain ketoacid dehydrogenase, causing accumulation of leucine, isoleucine and valine. It presents with a characteristic urine odour, poor feeding and neurological decline.

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Wilson disease is a disorder of copper metabolism with low ceruloplasmin, causing copper accumulation in the liver, brain and cornea, where it forms Kayser-Fleischer rings. Treatment uses copper chelators such as penicillamine.

Explanation

G6PD deficiency, an X-linked disorder, reduces NADPH and leaves red cells vulnerable to oxidative stress. Triggers such as fava beans, infections and drugs like primaquine cause haemolysis with bite cells and Heinz bodies.

Explanation

Homocystinuria, most often from cystathionine beta-synthase deficiency, causes a marfanoid habitus, downward lens dislocation, thromboembolism and intellectual disability. In Marfan syndrome the lens dislocates upward and there is no thrombotic tendency.